RED BLOOD PATHOLOGYdo.rsmu.ru/fileadmin/user_upload/lf/RED__BLOOD...Erythrocyte sedimentation rate -...
Transcript of RED BLOOD PATHOLOGYdo.rsmu.ru/fileadmin/user_upload/lf/RED__BLOOD...Erythrocyte sedimentation rate -...
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RED BLOOD PATHOLOGY
ANEMIAS
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Plurpotential stem cells
Common myeloid stem cells Lymphopoietic stem cells
Commited progenitors of erythrocytes, granulecytes, monocytes, megakariocytes
Commited progenitors of B-lymphocyte and T-lymphocyte classes
Immature hemopoietic precusors
Immature lymphocyte precusors
Mature functional blood cells Mature functional lymphocytes
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ROLE of ERYTHROPOIETIN in REGULATION of ERYTHROPOIEsIS
Decreased production of mature RBC-s Decreased Hb synthesis, Decreased blood flow , Hemorrhages, Increased oxygen consumption by tissues.
Decreased arterial PO2 ↓ O2 content in tissue cells
Hypoxia of kidney ↑ secretion of erythropoietin by UGA of kidney
↑ proliferation of erithroblasts in bone marrow
↑ population of reticulocytes in circulation
↑ arterial PO2
↓ secretion of erythropoietin
↑ mature erythrocytes in circulation
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Erythrocyte sedimentation rate - ESR Panchenkov method, Westergren method
AGE Children WOMEN MEN
Midle age 10 -12 mm/h 2 – 20 mm\h
8-10 mm/h 1 – 10 mm/h
>50 women > 60 men
15 mm/h (avar) 14 -25 -30 mm/h
18-20 mm/h
1 month 1 - 6 years old > 8 years old
2 – 30 mm/h 1 – 12 mm/h as in adult
Causes of ↑ESR : inflammation, intoxication, acute , chronic infections, trauma, myocardial infarction, autoimmune diseases, anemia, blood loss, tumor diseases, pregnensy Causes 0f ↓ESR: ↓ body mass, dehydration, glucocorticoids , starvation, Poyicytemia Vera.
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PRICE – JOHNS’s CURVE
normal size of erythrocyte
macrocytes megalocytes Diameter
microcytes
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FOOD SOURCES of the major HEMATINICS
(all uncooked mean values) Products Fe
mg/100g FOLATE mg/100g
VITAMINE B12
MEAT 3 10 5
LIVER 10 300 100
FLOUR 1,5 - 7 14 - 20 0,4
GREEN VEGETABLES 10 50 0
MILK 0,2 0,2 0,2 – 0,6
EGGS 2 8 1/egg
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ANEMIA - is a clinic –hematologic syndrome which characterized by decreasing in hemoglobin and/or Erythrocyte number in the unit of blood volume
ANEMIA commonly result from : 1. Impaired erythrocyte production , 2. blood loss (acute or chronic) 3. increased erythrocyte destruction 4. combination of these three
RI Reticulocytic index
Color index
CI normal = 0.86 – 1.05
RI normal = 2
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CLASSIFICATION OF ANEMIA DUE TO TYPE OF ERYTHROPOEISIS:
MEGALOBLASTIC anemia: B12 - folate deficiency, - Folate deficiency NORMOBLASTIC : all others anemia
DUE TO the level of saturation of erythrocyte with hemoglobin
- Normochromic normal MCHC= 31-36 gm/dl (hemolytic A) CI = 0.85 -1.05 - Hypochromic MCHC < 31 gm/l ( iron-deficiency A) CI < 0.85 -Hyperchromic MCHC > 36 gm/l (B12 -folate deficiency A) CI > 1.05
DUE TO SIZE of ERYTHROCYTES: -Normocytic MCV = 86 -100fi (hemolytic anemia) - Microcytic MCV < 86 fi (iron deficiency anemia) - Macrocytic MCV > 100 fi (B12 folate deficiency anemia
DUE TO REGENERATIVE ABILITY OF BONE MARROW
Hypo-regenerative IR < 2, Regenerative IR =2, HYper-regenerative IR > 2
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CLASSIFICATION of ANEMIAS: DUE TO ETIOLOGY AND PATHOGENESIS:
Anemia (A) of impaired erythropoiesis: - Altered hemoglobin synthesis: iron deficiency A, Thalassemia, - Sideroblastic A , Sickle-cell A - A of chronic diseases - Altered DNA synthesis: B12 –deficiency, Folate-deficiency A - BONE MARROW FAILURE (or replacement): - Aplastic anemia, - Myeloproliferative leukemia - Anemia of increased erythrocyte destruction :
Hemolytic anemia - ANEMIA OF BLOOD LOSS: acute post-hemorrhagic A , chronic post-hemorrhagic A
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POSTHEMORRHAGIC ANEMIAS CAUSES: acute or chronic blood loss
STAGES of acute post hemorrhagic anemia
1. Hidden A. or DUE TO reflex OF SYMPATHETIC NERVOUS SYSTEM – (hours/1day) ↓ blood volume, ↓erythrocytes
and leukocytes, MCH, MHCH , Ht, color index are N
2. Hydremic – ( 1-2 days) blood volume restored due to plasma - oyigocytemia normovolemia, ↓ Er, ↓ Hb, ↓ Ht , ↓Rt
3. REGENERATIVE or activation of bone marrow regeneration – (4-5 days) - hypoxia of kidney → activation of UGA → →↑erythropoietin → activation of bone marrow regeneration → ↑ Rt, but ↓Hb, ↓Ht,↓ color index neutrophilia with regenerative shift to the left, thrombocytosis.
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Acute post hemorrhagic anemia
is normoblastic,, normochromic - color index –N, MCH, MCHC – N normocytic –MCV-N, regenerative (reticulocytosis, neutrophilia with regenerative shift to the left, thrombocytosis in 3-d stage
CHRONIC POST HEMORRAGIC ANEMIA Appear due to repeated insignuficant blood loss. Causes: hemorrhoid, uterine blood loss, ulcer disease and ets. Consequence : ↓ iron stores in organism (iron deficiency anemia) and impaired regeneration capacity of bone marrow.
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IRON (Fe) CICLE
Bone marrow
erythrocytes
secreted with bile
blood stream aged, abnormal or damaged erythrocytes
macrophages in spleen, liver, bone marrow
IRON + TRANSFERRIN
Hb
bilirubin Fe
heme globin
storage in liver
release
IRON reused in the synthesis of new erythrocytes
storage in spleen
≈ 67 % of total body iron is bound to heme in erythrocytes and muscle cells ≈30 % is stored bound to ferritin of hemosiderin in macrophages ≈ 3 % (less than 1 mg) is lost daily in urine, sweat, bile, epithelial cells shed from GIT. IRON not lost is continiously recycled
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METABOLISM OF IRON
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Causes of iron deficiency anemia
Impaired of Fe reabsorbton: gastroectomia, diseases of thin intestine, SPROU, achlorhydria
Chronic BLOOD LOSS: ulcer diseases, excessive menorrhages, Kron’s disease, tumors in GIT, hematuria
Insufficient dietary intake of Fe
Chronic diseases
↑ demand for iron
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- Acute erosious Gastritis -Duodenal ulcer -Fe malabsorption -severe vegetarian
Causes of iron deficiency anemia
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Causes of iron deficiency anemia
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DEFICITE OF IRON IN ORGANISM
↓ ham synthesis
↓ Hb formation
↓ synthesis of Fe-containing enzymes, myoglobin
ANEMIA
Damaged organs and tissue
↓ activity of antioxidant system
↑ lipid peroxydation
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hypochromic er.
IRON DEFICIENCY ANEMIA poikilocytosis –various shape
anisocytosis – various size
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IRON DEFICIENCY ANEMIA
HYPOCHROMIA, MICROCYTOSIS, single target shape erythrocyte
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IRON DEFICIENCY ANEMIA
CLINICAL SYMPTOMS and SIGNS: - Fatigue and sleepiness - Dyspnea - Brittle nails - Koilonychias (spoon-shaped nails) - Sore tongue - Angular stomatitis - ( Indolent crackings at the corner of the mouth) - Dysphagia - Pica (abnormal taste) - Pallor
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IRON DEFICIENCY ANEMIA. CLINICAL manifestations
SYNDROME of SIDEROPENIA: Dry skin, early loss of hear, glossitis, “pica chlorotica” - abnormal taste. Kollonychias The nail s are brittle, thin, spoon-shaped as a result of impaired capillary circulation and cellular breathing (↓ activity of enzyme- cytochromoxydase ).
Atrophic changes in GIT : gastritis, enteritis, ↓HCl secretion → malabsorption
Pallor of the skin and mucous membrane.
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Symptoms of IRON deficiency ANEMIA
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Treatment of IDA
1. To identify and eliminate the sources of blood loss. 2. Iron replacement therapy is very effective in the treatment of IDA and usually continued for 6 - 12 moths after bleeding. Iron preparation are administrated orally, i/v, i/m 3. Take iron tablets with vitamin C 4. Diets with ↑ iron in products only for
prophylactic IDA
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SIDERBLASTIC ANEMIA Hereditary (linked with X chromosome) Acquired due to poisoning by lead (Pb) or hypovitaminosis B6 ,
intake of drugs (untituberculosis), alcoholism, copper deficiency.
Pathogenesis: hereditary or acquired deficit of enzymes , which take part in porfirin and protoporfirin synthesis
SIDEROBLASTIC ANEMIA IS NORMOBLASTIC< HYPOREGENERATIVE MICROCYTIC HYPOCHROMIC
CLINICAL MANIFESTATION: hypoxic syndrome , impaired function of organs , in which appear hemosiderosis and dystrophy
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HEME STRUCTURA
HEME SYNTHESIS
SUKcinil KoA + glycin ð –aminolevulinat
PB syntase ð –aminolevulinic acid porfobilinogen synthasa Porphobilinogen Uroporphinogen 111 CO2 decarboxylase Coproporphinogen 111 oxidase Vit.B6 Protoporphinogen 1X Oxidase Protoporphirine 1X Fe ferrohelatase HEME
mito
cho
nd
ria cytop
lasm
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Lead poisoning - sideroblasts – ring form
Peripheral blood in Sideroblastic anemia: myicrocytic, hypochromic, Hyporegenerative, normoblastic
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COMPARISON of IRON –DEFICIENCY and SIDEROBLASTIC anemia
Laboratory test Iron deficiency anemia
Ring-form
serum iron ↓ < 12 µm ↑ > 30 µm
Total iron binding capacity ↑ ↓
Ferritin in serum ↓ ↑
Transferrin saturation ↓ ↑
Siderophags in blood stream ↓ ↑
Sideroblasts in bone marrow ↓ ↑ ring - form
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Treatment of sideroblastic anemia.
Imdividuals with hereditary SBA are usually treated with pyridoxine therapy in doses of 50 up 200 mg per day . One third of persons with hereditary SBA respond to this therapy. For individuals who do not respond to pyridoxine, blood transfusion are necessary . Individuals who demonstrate evidence of iron overload need to iron depletion therapy to prevent organ damage. Individuals with acquired SBA respond to pyridoxine
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HEMOLYTIC ANEMIAS
CLASSIFICATION: HEMOGLOBINOPATHIES: Thalassemia α and β (congenital) Sickle cell anemia ENZYMOPATHIES: Glucose- 6-phosphate dehydrogenase (congenital) deficiency MEMBRANOPATHEIS (ERYTHROCYTOPATHIES): (plasma membrane of erythrocyte is affected) Hereditary form: Acquired forms Spherocytosis - immune : Drug-induced forms (hapten model) - hemolytic anemia of newborn (mother Rh “-”, fetus Rh “+” ) - Non- immune: -Transfusion reactions, caused by ABO incompatibility - Idiopathic hemolytic anemia
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Hemolytic anemia: normocyting (MCV)
normochromic (MCHC), Hyper regenerative
Hemoglobinuria leg ulcers
gall stones
anemia Jaundice Splenomegaly
Cranial overgrowth
extension of bone marrow
Feature s of hemolysis: reticulocytosis, ↑ iron + ↑bilirubin ↓ osmotic resistance
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PERIPHERAL BLOOD. RETICULOCYTOSIS
RETICULOCYTOSIS is CHARACTERISTIC of ALL HEMOLYTIC ANEMIAS
reticulocyte
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Sickle cell anemia
Sickle cell anemia is a hereditary disease characterized by the presence of abnormal form of hemoglobin - Hb-S. Hb S is formed by genetic mutation in recessive allele which encode the β- chain of protein hemoglobin: amino acid –valin- replaces glutamic acid.
Hb S → deoxygenation → hypoxia → dehydration → solidifying → stretching of erythrocyte into elongated sickle shape
Causes: spontaneous mutation and deletion of ß – globin gene on 11 chromosome lead to HbS synthesis .
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SICLE CELL ANEMIA
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Brain: hemorrhage thrombosis
- splenic infarcts -skeletal defects -kidney hematuria - abdominal infarcts
-Dactylitis bone infarcts osteomyelitis - leg ulcers
SICKLE – CELL ANEMIA
Hypoxia, Acidosis Abdominal pain Fever Strokes Painful swelling of the hands and feet Dehydratio n Thrombotic crisis
Sickling
Clinical manifestations
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PATHOGENESIS of sickle –cell anemia
Replacement of glutamic acid to valin in b- chain of HB
Formation of hemoglobin -S
Aggregation and solidifying of Hg under the influence of hypoxia → sickle shape of erythrocytes
Rapid damage of erythrocytes. Disturbance of microcirculation
Anemia Stasis Microthrombi in lung and kidney Hepatomegaly, splenomegaly
Hypoxia stimulates bone marrow → activation of erythropoesis
Heperplasia of bone marrow. Pain syndrome
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MICROCPHEROCYTOSIS - hereditary hemolytic anemia
spectrin
ankirin
erythrocyte plasma membrane
glyciforin
actin
Spherosytosis appears due to mutation of gens, which controls the proteins in erythrocyte membrane: spectrin and ankerin. These proteins make contacts with cellular membrane and cytockeleton. When spectrin and ankerin are defected or absent affected erythrocytes decrease the length of plasma membrane ( ↓ cellular diameter) and increase permeability for Na.
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MICROSPHEROCYTOSIS : normoblastic,
hyperregenerative
Deficiency in membrane proteins leads to a very low erythrocytes deformity → they destroy in spleen → splenomegaly
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APLASTIC ANEMIA PANCYTOPENIA - reduction or absent of all three types of blood cells. It results from failure or suppression of bone marrow to produce an adequate amounts of blood cells
Aplastic anemia : normoblastic, a (hypo)-regenerative, normocytic, normochromic (MCV, MCH, MCHC –N) CAUSES: radiation, toxic substances, some drugs, severe viral infections, metastasis of tumor cells, autoimmune process, mediated by TNF and INFÝ product of T-lymphcyts and NK. CLINICAL MANIFESTATIONs appear due to tree syndromes - hypoxic (↓ Er, ↓Hb), - hemorrhagic (↓Trc) - immuno-depression (↓NP, ↓LP)
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Bone marrow NORMAL APLASTIC ANEMIA – pancytopenia
CLINICAL MANIFESTATIONS: Hypoxic syndrome Hemorrhagic syndrome Immunodepressive syndrome -pallor, -severe weakness, -hemorrhaging, infections.
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Normal bone marrow Bone marrow in Aplastic anemia
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B12 – FOLATE DIFICIENCY ANEMIA
↑MCV - macroergic, ↑MCH –C hyperchromic, hyporegenerative
PERIPHERAL BLOOD: ↓erythrocytes (macrocytes, megalocytes), ↓ reticulocytes, ↓ plateletes, ↓ lymphocytes, ↓ osmotic resistance, Jolly bodies, Cabot rings, ↑ Fe + ↑billirubine→ Hemolysis BONE MARROW: packed with red cell precursors , megaloblasts
B 12 – DEFICIENCY FOLATE DEfICIENCy Absorption: terminal ileum jejunum B12 + intrinsic factor
CLINICAL MANIFESTATIOS: megaloblastic anemia, jaundice, Disturbance in gastro-intestinal tract: -glossitis (tongue is glazed, beefy) - atrophic gastritis (autoimmune atrophy of fundice glands)
NEUROLOGIC SYMPTOMS -----------------------
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VITAMIN B12
Methylcobalamine Adenosilcobalamine
FOOD FOLATES
Methyl THF Uridine nonophosphate
THYMIDINE synthesis
PYRIMIDINE
DNA SYNTHESIS
THF
Methylmalonic KoA
Cuccinyl KoA
Krebs cycle
Succinic acid
Methylmalonic acid
B12 - and Folates metabolism are interrelated
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CAUSES of B12 –deficiency anemia
INADEQUATE INTAKE: severe vegetarianism Extreme malnutrition MALABSORPTION gastric: - gastric atrophy, - congenital intrinsic factor deficiency -partial or total gastroectomia 0 cancer of the stomach MALABSORPTION intestinal: ileum resection, - Tropical sprue, - fish tapeworm ( diphillobothrium) - - Kron disease, - deficit of receptors for B12 + IF
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B12 deficiency anemia. Symptoms
Gray hair Blue eyes Reticulopathy Jaundice Sore, smooth tongue Tiroid disease
splenomegaly Addison’s disease ? Diabetes ? Vitiligo
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GLOSITIS . Tongue of patient with B12 (folate) deficiency anemia appear due to loss of DNA synthesis → reduced proliferation of tongue epithelium. NEUROLOGIC SYMPTOMS in patient with B12 deficiency anemia are the result of nerve demyelination or nerve cell death due to toxic effect of metylmalonic acid
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Pernicious anemia is the most common type of B12 megaloblastic
anemia
CAUSE of pernicious anemia - absent of intrinsic factor - an enzyme required for absorption of dietary vitamin B 12
Autoimmunity plays a significant role in the development Of pernicious anemia, characterized by the presence of autoantibodies to gastric parietal cells, which can secrets intrinsic factor.
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DIPHILLOBOTRIOSIS
Disbacteriosis
Disturbance of vitamin B 12 biosynthesis
Absorption of vitamin B 12 by parasites
Aditional factors: unbalance feeding, decreased synthesis of intrinsic factor, fever, pregnansy
Hypovitaminosis B 12
B 12 deficiency anemia
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B12 -FOLATE DEFICIENCY ANEMIA
PERIPHERAL BLOOD
1- Macro,- megalocytes, 2 – erythrocytes with Jolly bodies, 3- normocytes, 4- Poly chromic erythrocytes
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Blue bone marrow B 12 deficiency anemia
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Cabot ring
Jolliy body
Hyper--segmented NP
Hyperchromic erythrocytes
B12 (folate) deficiency anemia
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Treatment of B12 - Folate - deficiency anemia
Replacement of vitamin B12 (cobalamine) oral Individuals with atrophic gastritis need to i/v injection of vitamin B 12
Individuals with Folic deficiency anemia require daily oral administration of folate preparations 1 mg/day
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POLYCYTHEMIA VERA
is a neoplastic, nonmalignant chronic myeloproliferative disease, which characterized by abnormal proliferation of bone marrow stem cell despite normal to below normal erythropoietin level . Mutation s in JAK2, CALR, rarely LVK in hematopoietic stem cells.
The most likely cause of PV is acquired genetic alterations in the stem cell leading to disturbance of normal cellular growth.
↑RBC, ↑WBC, ↑ platelets
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POLYCYTHEMIA VERA
Bone marrow Peripheral blood
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Hemoblastosis - instant erythremia
Polycythemia vtra
Clinical manifestations: Erythrocyanosis, ↑BP, thrombosis, bleeding ↑Er, ↑ granulocytes, ↑Ht, ↑ platelets, ↓ESR Hepatomegaly, splenomegaly