Folic Acid and Reticulocytosis Quiz

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Questions and Answers

Quale de iste conditiones es un facto contributivo a reticulocytosis?

Ipothyroidism / myxedema (correct)

Maladia de Crohn

Aumento de vitamina B12

Anemia ferropenica

Qual es un signo caracteristic de consumo excesivo de alcohol in relation a MCV?

MCV inferior 80

MCV non superante 110 (correct)

MCV superante 110

MCV intermedio 90-100

Quale de iste enfermedades es associata con reticulocytosis?

Artrite reumatoide

Diabetes mellitus

Sindrome myelodysplastic (correct)

Alzheimer

Quale de iste istatistiche non indica un facto de reticulocytosis?

Consumo de acidos grassos Signup and view all the answers

In qual caso MCV es probabile non superante 110?

Anemia microciter Signup and view all the answers

Quantos milligrams de folato le corpore se conserva in le hepate?

10-12 mg Signup and view all the answers

Dove folic acid es principalmente assorbite?

Jejunum Signup and view all the answers

Quale de le sequente non es un causa de carentia de folic acid?

Consumo excessive de proteinas Signup and view all the answers

Quale stato de salve non demanda un augmento in folic acid?

Sportivitas intensa Signup and view all the answers

Quale malady es associada con malabsorptione de folic acid?

Celiac disease Signup and view all the answers

Qual es le forma normal de cellulas rubras que le medulla ossea produce?

Biconcave Signup and view all the answers

Que happen a cellulas rubras durante lor circulation in le systema RE?

Perde membrana e deveni spherical Signup and view all the answers

Qual es le consequence del perdita de superficie relativa durante le circulation de cellulas rubras?

Reduction de efficacia pro transporto de gas Signup and view all the answers

Cual organo es implicate in le modification de cellulas rubras post-production?

Le sleen Signup and view all the answers

Que resulta del circulo de cellulas rubras per le sistema RE?

Deveni spherical e minor in superficie Signup and view all the answers

Qual es le consequence de un absentia de secrezione de fator intrinseco (IF)?

Deficientia de vitamina B12 Signup and view all the answers

Le que occurre quando there es achlorhydria in le organismo?

Reducte de secretion de pepsina Signup and view all the answers

Quo causa le deficiency de vitamina B12 in le context de achlorhydria?

Absente de secreto de facteur intrinseco Signup and view all the answers

Como le corpo es affectate pro le absentia de vitamina B12?

Sviluppo de anemia megaloblastica Signup and view all the answers

Quo es le rol de vitamina B12 in le corpore?

Sustenta la formation de glóbulos rubros Signup and view all the answers

Qual es le causa principal del morte premature de spherocites in hereditari spherocytosis?

Le incapacitá de passar per le microcirculation Signup and view all the answers

Qual statement es ver si considera hereditari spherocytosis (HS)?

Es le forma plus commun de anemia hemolytica hereditari in le europaeos del nord. Signup and view all the answers

Qual es le consequence de le liberamento de partes del bilayer lipidic?

Le lassamento de membrane e hemolysis. Signup and view all the answers

In le context de hereditari spherocytosis, qual organo es particolarmente implicate in le morte de spherocites?

Le spleen Signup and view all the answers

Qual es le resultato de le morte premature de spherocites?

Le development de anemia hemolytica. Signup and view all the answers

Quale condition se presenta con una severe anemia emolytica in pacientes con elliptocytosis?

Hereditari pyropoikilocytosis Signup and view all the answers

Quale caracteristica describe le cellulas in South East Asian ovalocytosis?

Cellulas rigid e resistente a invasion Signup and view all the answers

Quale statement se considera false in relation a elliptocytosis?

Le evidenti de hemolysis es sempre apparent. Signup and view all the answers

Quale tipo de anemia es causate per hereditari pyropoikilocytosis?

Anemia emolytica severa Signup and view all the answers

Quale de le sequente caracteristicas non es asociate a elliptocytosis?

Geographic concentration in Europa Signup and view all the answers

Study Notes

Hematology Lecture Notes

Course: Hematology
Lecturer: Dr. Sura Al Shamma
Department: Pathology
Year: 2024

Macrocytic Anemias

These anemias feature red blood cells (RBCs) with mean corpuscular volume (MCV) greater than 98 fl.
Two types of macrocytic anemias exist:
- Megaloblastic anemia
- Non-megaloblastic macrocytic anemia

Non-Megaloblastic Macrocytic Anemias

These conditions result from factors other than vitamin B12 or folic acid deficiency.
Red blood cells (RBCs) in these conditions are round.
Conditions leading to round macrocytes:
- Reticulocytosis
- Hypothyroidism/myxedema
- Myelodysplastic syndrome
- Scurvy (vitamin C deficiency)
- Liver disorders
- Alcohol excess (with MCV not exceeding 110)
- Congenital dyserythropoietic anemia (CDA I and III)
- Erythroleukemia
- Neonates

Megaloblastic Anemia

This anemia group is characterized by abnormal erythroblasts in bone marrow.
Maturation of the nucleus is delayed relative to the cytoplasm in erythroblasts.
Caused by vitamin B12 or folic acid deficiency.
The underlying defect relates to DNA synthesis errors during cell maturation.
Macrocytes in this condition are usually oval, hence termed macro-ovalocytes.

Causes of Megaloblastic Anemia

Vitamin B12 deficiency
Folate deficiency
Abnormalities in vitamin B12 or folate metabolism (e.g. transcobalamin deficiency, nitrous oxide, or antifolate drugs)
Other defects in DNA synthesis
Congenital enzyme deficiencies (e.g., orotic aciduria)
Acquired enzyme deficiencies (e.g., alcohol, therapy with hydroxyurea, or cytosine arabinoside)

Vitamin B12

Dietary sources: Primarily meats, fish, eggs, and dairy products.
Daily requirement: Approximately 1-2 µg in adults.
Body stores: 2-3 mg stored in the liver (sufficient for 2-4 years).
Absorption: B12 binds to proteins in foods, released in the stomach by acid and pepsin, and then binds to intrinsic factor (IF) and absorbed in the terminal ileum.
Deficiency Causes: Autoimmune gastric atrophy (leading to decreased IF production), gastrectomy, ileal resection, ileitis, Zollinger-Ellison syndrome, blind loop syndrome, fish tapeworm infestation, and pancreatic insufficiency.

Vitamin B12 Absorption (Mechanism)

B12 binds to proteins in foods.
Stomach acid and pepsin release B12 from proteins.
Stomach lining cells release intrinsic factor (IF).
IF binds to B12 in the small intestine.
B12-IF complex binds to receptors in the ileum, allowing absorption.
Some un-bound B12 may be absorbed by passive diffusion.

Folate

Dietary source: Present in green vegetables, fruits, meat, and liver.
Daily adult needs: 100-150 µg
Body stores: 10-12 mg stored in the liver (sufficient for 3-4 months).
Absorption: Primarily absorbed in the jejunum.
Factors affecting folate availability : Decreased intake, increased demand (pregnancy, hemolysis, hemodialysis, malabsorption, and disorders interfering with folate metabolism).

Clinical Features of Megaloblastic Anemia

Gradual onset of anemia symptoms.
The hallmark is defective DNA synthesis in rapidly dividing cells in bone marrow and other tissues.
Macrocytic cells appear on blood count.
Potential symptoms include shortness of breath, muscle weakness, pale skin, loss of appetite/weight loss, diarrhea, nausea, fast heartbeat.

Clinical Features of Megaloblastic Anemia (Specific Signs)

Glossitis (swollen, beefy tongue).
Jaundice and splenomegaly (due to excess breakdown of hemoglobin from ineffective erythropoiesis).
Peripheral neuropathy/paresthesia.
Dementia.
Loss of vibratory and positional sense/ataxia.
Neural tube defects in neonates (folate related).
Purpura (less frequent).

Pernicious Anemia

An autoimmune disorder causing vitamin B12 deficiency.
Common among Northern Europeans, frequently seen in people aged 60-70 years.
Characterized by chronic gastric inflammation leading to atrophy, diminished or absent intrinsic factor (IF) production.

Laboratory Diagnosis for Macrocytic Anemias

Blood count: Reduced hemoglobin, MCV above 100-110 fl, presence of ovalocytes
Serum vitamin B12: Decreased level.
Serum and erythrocyte folates: Decreased levels.
Homocysteine and Methylmalonic acid: Increased levels.
LDH, Bilirubin (unconjugated): Increased levels

Hemolytic Anemias

Mechanism: Result from increased red blood cell (RBC) destruction. Two mechanisms: intravascular (RBCs broken down directly in circulation) or extravascular (excessive removal by the reticuloendothelial system).
Causes: Hereditary (defects like membrane or metabolic disorders, hemoglobin abnormalities) or acquired (immune-mediated destruction, infections, drugs, physical injury).

Clinical Features of Hemolytic Anemia

Jaundice: Result of increased bilirubin production
Pigment gallstones: Due to excess bilirubin
Hepatosplenomegaly: Caused by extramedullary hemopoiesis (bone marrow outside of the bone).

Mechanisms of Red Cell Destruction

Extravascular: Excessive removal of RBCs by cells of the reticuloendothelial system.
Intravascular: RBC lysis directly within the circulation causing haemoglobinemia and hemoglobinuria.

Laboratory Findings for Hemolytic Anemia

Features of increased red cell breakdown: Increased serum bilirubin, increased urine urobilinogen, decreased/absent serum haptoglobin.
Features of increased red cell production: Reticulocytosis, bone marrow erythroid hyperplasia.
Damaged red cells: Microspherocytes, elliptocytes, fragments, osmotic fragility tests, and specific enzyme, protein, or DNA tests.

Hereditary Hemolytic Anemias

Membrane defects: Congenital spherocytosis, hereditary elliptocytosis, hereditary stomatocytosis, and others).
Metabolic defects: Glucose-6-phosphate dehydrogenase (G6PD) deficiency, and Pyruvate kinase (PK) deficiency.
Hemoglobin defects: Sickle cell anemia and thalassemia.

Specific Hereditary Hemolytic Anemias

Hereditary Spherocytosis (HS): Common in Northern Europeans and characterized by spheroid red blood cells (RBCs). Related to defects in membrane proteins (e.g., spectrin, ankyrin).
Hereditary Elliptocytosis: Less severe than HS and features elliptical RBCs.
Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency: X-linked genetic disorder impairing NADPH production in RBCs, increasing cell susceptibility to oxidant stress (like fava beans).

G6PD Deficiency

Inheritance: X-linked, primarily affecting males.
Mechanism: Deficiency of the enzyme G6PD affecting NADPH production.
Precipitants: Drugs, infections, fava beans, and others.
Clinical features: Acute hemolytic episodes due to oxidant stress; often asymptomatic.

Pyruvate Kinase Deficiency

Inheritance: Autosomal recessive.
Mechanism: Deficiency in the enzyme that generates ATP in RBCs, leading to premature cell death.
Clinical features: Chronic hemolytic anemia, often with microspherocytes on blood smears; often with increased reticulocytes.

Laboratory Findings for G6PD Deficiency

Normal blood count between crises.
Enzyme deficiency detectable by screening tests or direct enzyme assays.
Abnormal blood film in crisis (e.g., contracted/fragmented cells, bite and blister cells).
Elevated bilirubin (unconjugated).
Other laboratory tests might include elevated LDH.

Treatment for Haemolytic Anemias

General Measures: Treating underlying infections. Discontinuing offending drugs.
Specific Measures: Blood transfusion for severe cases. Splenectomy (for conditions like HS)

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Description

Este quiz examina diferentes aspectos de la reticulocytosis y su relación con el ácido fólico. A través de preguntas sobre condiciones, deficiencias y el proceso de producción de células rojas, se evalúa el conocimiento sobre este tema importante en la hematología.