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Hematology tests
This review version of the Diagnostic Clinical Hematology Test Examination has compiled the key and difficult points in general blood tests, laboratory tests for anemia, bone marrow cytology tests, and blood characteristics of common hematological diseases. If there are any disputes, please point them out to teachers and students.
Edited at 2023-02-15 09:45:20- bacteria
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Hematology tests
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clinical hematology tests
General testing of blood
General blood tests related to red blood cells
Red blood cell/hemoglobin measurement
Male: 4.0–5.5*10^12/L
Men: 120–160g/L
Female: 3.5–5.0*10^12/L
Women: 110–150g/L
Children: 6.0–7.0*10^12/L
Children: 170–200g/L
Quantity change
Increased red blood cells and hemoglobin
Male red blood cells>6.0*10^12, hemoglobin>170g/L; female red blood cells>5.5*10^12, hemoglobin>160g/L
Relative increase: Relative increase caused by loss of body fluids, such as severe diarrhea, dehydration, and extensive burns
Primary polycythemia: polycythemia vera
Secondary increase: hypoxia, plateau, chronic severe pulmonary heart disease
Decreased red blood cells and hemoglobin
Physiological reduction: Infants, young children, some elderly people, and pregnancy may experience a reduction in red blood cells and hemoglobin.
Pathological reduction: seen in individual types of anemia resulting in a decrease in red blood cells
Red blood cell morphological changes
Normal red blood cell morphology: biconcave size is relatively consistent, disc-shaped, diameter 6-9um
Abnormal size
small cells
<6um is generally seen in hypochromic anemia. For example, in iron deficiency anemia, the central staining area will expand.
large cells
>10um is generally seen in lytic anemia, blood loss anemia, and also in megaloblastic anemia.
giant red blood cells
>15um is generally seen in giant infantile anemia due to folic acid and vitamin b12 deficiency.
Uneven size of red blood cells
Abnormalities during red blood cell proliferation, common in megaloblastic anemia
Abnormal morphology
Target cell, globinogenic anemia, dyshemoglobinopathies
Teardrop cell, myelofibrosis, hemolytic anemia
Acanthocytes, post-splenectomy, uremia
Schist cell, DIC extensive burns
Red blood cells arranged in a coiled pattern, multiple myeloma
Abnormal coloring
low pigment
Common in iron deficiency anemia and globin production disorder anemia
Highly pigmented
Generally seen in megaloblastic anemia, spherical cells are also hyperpigmented
pleochrophilia
After staining, they appear gray-blue or gray-red, which are actually reticulocytes. The increase indicates active hematopoietic function.
Seen in proliferative anemia, especially anemia
Structural abnormality
Basophilic stippling
Lead poisoning, giant child poverty
chromatin body
Poverty alleviation, huge child poverty
kabo ring
Lead poisoning, megaloblastic anemia, hemolytic anemia
nucleated red blood cells
Anemia, erythroleukemia, extramedullary hematopoiesis
Detection of reticulocytes
The erythrocyte stage in which the late erythrocytes shed their nuclei but still retains ribosomes, which is named after the light blue or dark blue mesh with brilliant tar blue and new methylene blue.
Reference
Adults and children: 0.5%-1.5%
Newborns: 3%-6%
clinical significance
Cytosis: Indicates strong proliferation of red blood cells in the bone marrow, which is common in anemia, anemia, iron deficiency anemia, megaloblastic anemia, etc.
Cytopenia: generally indicates aplastic anemia, pure red blood cell aplasia
White blood cell test
normal white blood cells
Adult: (4–10)*10^9/L
Newborn: (15–20)*10^9/L
6 months to 2 years old: (11–12)*10^9/L
In adults, a value higher than 10*10^9/L is called leukocytosis; a value lower than 4*10^9/L is called leukopenia.
Classification
eosinophils
Physiological functions: inhibit allergies and helminth reactions
Absolute increase in cell count: parasitic diseases, allergies, skin diseases, scarlet fever, etc.
Reduce: typhoid fever, paratyphoid fever, etc.
basophils
Physiological function: mediates hypersensitivity
Increased cells: allergies, chronic myeloid, metastatic cancer
Lymphocytes
Increase: graft immune rejection
Reduce: congenital or acquired immunodeficiency diseases, long-term use of glucocorticoids, etc.
monocytes
Increased: seen in blood diseases (lymphoma, MDS, etc.), infections (tuberculosis, endocarditis)
neutrophils
Peripheral blood generally contains rod-shaped nucleated granulocytes and lobulated nucleated granulocytes.
When the absolute value of neutrophils is less than 1.5*10^9, it is called agranulocytopenia; when the absolute value of neutrophils is less than 0.5*10^9, it is called agranulocytosis;
Quantity change
increase
Physiological: There is a temporary increase in neutrophils in the afternoon than in the morning, pregnancy and childbirth, strenuous exercise, high temperature and cold, etc.
Pathological: acute infection, acute poisoning, leukemia, massive bleeding, tissue damage, etc.
reduce
Infections, hematological diseases, physical-chemical injuries, hypersplenism, autoimmune diseases
nuclear image changes
nuclear left shift
Refers to the percentage of non-lobulated nuclei exceeding 5%, which is called left shift
Mild left shift usually indicates acute purulent infection, extreme left shift usually indicates leukemia or leukemia-like disease.
nuclear right shift
Granulocyte nuclei with five lobes or more and accounting for more than 3% are right-shifted
Mainly seen in megaloblastic anemia and decreased hematopoietic function, it can also indicate a poor prognosis.
Abnormal morphology
toxic changes
Uneven cell size, toxic particles, vacuolar degeneration, Dürer bodies
Nuclear degeneration (pyknosis, dissolution and fragmentation)
giant multilobulated neutrophils
Genetically related neutrophil morphological abnormalities
Platelet test
The platelet count reference value is 100–300*10^9/L, and the abnormal platelet ratio in peripheral blood is greater than 10%.
clinical significance
Thrombocytopenia
Decreased production: common aplastic anemia, acute leukemia, macroplasia
Excessive destruction and consumption: systemic lupus erythematosus, upper respiratory tract infection, neonatal thrombocytopenia, post-transfusion thrombocytopenia, DIC
Uneven distribution: splenomegaly, hemodilution (transfusion of large amounts of banked blood)
thrombocytosis
Commonly seen in myeloproliferative neoplasms, polycythemia vera, essential thrombocythemia, and acute hemolysis
Erythrocyte sedimentation rate ESR
Influencing factors
Plasma proteins: fibrinogen or globulin albumin - (accelerated erythrocyte sedimentation rate)
Fibrinogen is the most powerful procoagulant substance
red blood cells
(1) Number of red blood cells: the more, the slower the erythrocyte sedimentation rate
(2) Red blood cell morphology: when the red blood cells are spherical, sickle-shaped or severely uneven in size, the erythrocyte sedimentation rate will be slower.
(3) Aggregation state of red blood cells: Viruses, bacteria, etc. will reduce the surface charge of red blood cells and significantly increase the erythrocyte sedimentation rate.
Pathological changes
(1) Inflammatory diseases: acute bacterial inflammation, rheumatic fever, tuberculosis and chronic inflammation
(2) Tissue damage and necrosis: ischemic tissue necrosis: myocardial infarction
(3) Malignant tumors
(4) Hyperglobulinemia caused by various reasons: chronic nephritis, liver cirrhosis
(5) Anemia, diabetes, nephrotic syndrome, hypercholesterolemia
Determination of hematocrit and application of red blood cell related parameters
Hematocrit determination
PCV refers to the volume ratio of red blood cells in the blood, which is affected by changes in the size of red blood cells and plasma volume.
clinical significance
Increased PCV
Various reasons lead to blood concentration, reaching above 0.5 as a reference for rehydration
PCV reduction
It is seen in various anemias, but the size of blood cells may be abnormal, so it must be considered comprehensively.
Red blood cell average calculation
Red blood cell volume distribution width calculation
Poor laboratory testing
definition
Anemia occurs due to various reasons that shorten the survival time of red blood cells and increase or accelerate the destruction of red blood cells, but the hematopoietic function of the bone marrow cannot compensate accordingly.
Classification
RBC intrinsic factors (genetic or congenital)
(1) Defects in red blood cell membranes
(2) Defects in hemoglobin structure or production
(3) Red blood cell enzyme defects
RBC external factors (acquisition)
extravascular hemolysis
Cause
Commonly seen in hereditary spherocytosis, hemoglobinopathies, and warm antibody autoimmune hemolytic anemia
Extravascular hemolysis: mostly chronic, manifested by: anemia, jaundice, hepatosplenomegaly, strong tea urine (urobilinogen)
intravascular hemolysis
Cause
Blood type incompatibility transfusion, hypotonic solution transfusion PNH G-6-PD, cold antibody type autoimmune hemolytic anemia
Intravascular hemolysis: mostly acute, manifested by: anemia, jaundice, soreness in the lower back and limbs, soy sauce-colored urine, hemosiderinuria
Poverty Dissolution Screening Test
1||| Plasma free Hb determination
Plasma free hemoglobin is significantly elevated during intravascular hemolysis
2||| Serum haptoglobin assay
Reduced Hp: indicates the presence of hemolysis. It is significantly reduced during intravascular hemolysis.
Increased Hp: chronic infection, malignant tumor, trauma, rheumatoid arthritis, SLE
3||| Plasma methemoglobin albumin determination
Normal negative, severe intravascular hemolysis positive
4||| Urine hemosiderin determination (Rous test)
A positive test is seen in chronic intravascular hemolysis, and a negative test cannot rule out anemia.
5||| RBC Lifetime Determination (Best)
Normal RBC life span 25–32 days
Clinical significance: Labeled with 51Cr isotope, the half-life is <15 days, indicating that there is anemia
Testing for red blood cell membrane defects
RBC penetration fragility test
Red blood cell incubation osmotic fragility test
Autohemolysis test and its correction test
Enzyme defects can be determined
After normal human heparin-anticoagulated blood is placed in a 37°C environment for 24-48 hours, red blood cells are eventually destroyed due to energy consumption, that is, slight hemolysis occurs. When glucose and adenosine triphosphate (ATP) are added, different degrees of correction can be obtained
For the cause diagnosis of hemolytic anemia
(1) Hereditary spherocytosis is significantly increased and can be corrected with glucose and ATP.
(2) Other hereditary non-spherocyte hemolytic anemias can also be increased and can be corrected by glucose or ATP respectively.
(3) Pyruvate kinase deficiency, autoimmune hemolytic anemia, and increased PNH cannot be corrected by adding glucose, but can be corrected by adding ATP.
PNH inspection
PNH related concepts
A clonal disease characterized by acquired blood cell membrane defects, which can clinically manifest intravascular hemolysis, embolism, pancytopenia, etc., and sometimes bone marrow failure.
preliminary screening test
Characteristics of intravascular hemolysis: increased plasma free hemoglobin, decreased haptoglobin (Hp), hemoglobinuria and hemosiderin in urine
Diagnostic test
Acid hemolysis test (Ham test)
Sucrose water hemolysis test
Snake venom hemolysis test
CD55 and CD59 testing
immune hemolysis test
antiglobulin test
Both direct and indirect methods essentially detect cell surface antigens.
Clinical significance: Normal people show negative results. Positive results may be neonatal alloimmune hemolysis, SLE, RA, HD, etc.
Cold condensation test
Principle: The body has antibodies against its own red blood cells, which bind to the corresponding antigens at low temperatures, causing red blood cells to agglutinate. Especially at 4°C or 37°C, the agglutination disappears.
Reference value: titer <1: 40
A 4-fold increase in agglutination titer is more valuable for diagnosis
Clinical significance: Some AIHA, infectious mononucleosis, malignant lymphoma, etc. can be positive
Bone marrow cytology examination
Indications and detection methods
Indications
Abnormalities in peripheral blood cell number, composition and morphology
Unexplained fever, liver, spleen, and lymph node enlargement
Unexplained bone pain, bone destruction, abnormal kidney function, jaundice,
Observation after chemotherapy
Contraindications
Contraindications for coagulation factor disorders
Bone marrow examination procedures
Low-magnification microscopy: determine bone marrow proliferation; roughly count megakaryocytes; detect whether there are special cells
Oil microscope inspection: cell proliferation, cytoplasm and quantity of each cell line, observation of mature red blood cells, platelets, blood parasites, etc.
Five-level distribution to determine bone marrow hyperplasia
Blood cell production and development rules
Morphological evolution rules of blood cells during development
Normal morphological characteristics of red blood cells
primitive red blood cells
Cell body: round or oval, often with tumor-like protrusions on the edge
nucleus
Nucleoli: 1–3
Nucleus shape: round or oval
Nuclear chromatin: purple-red granular
Cytoplasm: small amount, dark blue, opaque, no particles
Early, middle and late red blood cells
Cell body: round or oval, with tumor-like protrusions visible on the edge
Nucleus: Nucleoli are mostly absent
Cytoplasm: abundant, dark blue (Early Young Red); polychromatic, blue-gray, gray-red (Medium Young Red); light red or gray-red (Late Young Red)
reticulocytes, mature red blood cells
granulocyte development
blasts
Cell body: round or quasi-round
nucleus
Nucleus shape: round or quasi-round
Nucleoli: 2–5 small and clear
Nuclear chromatin: finely granular
Cytoplasm: small amount, transparent staining or dark blue, no or less granules
promyelocytes
Cell body: round or oval
nucleus
Nucleus shape: round or oval
Nucleolus: blurred
Nuclear chromatin: coarsely granular
Cytoplasm: abundant, light blue or dark blue, containing abundant non-specific granules
Mesomyelocytes
Characteristics of the nucleus: oval, accounting for 1/2–2/3 of the cell volume, flat or sunken on one side; chromatin is in the form of cords; nucleoli are often absent; contains a very small amount of non-specific granules, with relatively obvious specificity particles
Neutral particles: medium amount, small and uniform in size, lavender or light red, difficult to see clearly with ordinary light microscope
Eosinophilic granules: thick, consistent in size, three-dimensional and refractive
Basophilic granules: appear in the cytoplasm and nucleus, are small in number, thick, varying in size, disorderly arranged, dark purple and black
promyelocytes
Characteristics of the nucleus: the volume accounts for less than 1/2 of the cell, is obviously sunken, horseshoe-shaped, kidney-shaped, half-moon-shaped, and the nucleolus disappears
Particle characteristics: Contains a small amount of non-specific particles and specific particles
rod-shaped granulocytes
Nucleus characteristics: The nuclear volume accounts for less than 1/2 of the cell, and is in the shape of a uniform band, S, U, or E shape.
lobulated granulocytes
It is lobed, with broken connections between leaves, and the chromatin is dark purple with many small patches.
mature lymphocytes
Cell body: round or oval
nucleus
Nucleus shape: round or nearly round with small notches,
Nuclear chromatin: tight chunks
Kernel: disappear, sometimes false kernel can be seen
Nucleoplasm: light blue large lymphocytes have more cytoplasm, small lymphocytes have less cytoplasm and often no granules.
mature plasma cells
Cell body: 8–15um
Nucleus: round or oval, accounting for less than 1/3 of the nucleus, chromatin is roughly arranged in a spoke shape, without nucleoli
Cytoplasm: Large amount, occasionally azurophilic granules can be seen, and the cytoplasm has a granular feel.
megakaryocyte development
granular megakaryocytes
Cell body: huge, the largest cell in the bone marrow, irregular in shape
Nucleus: huge, extremely irregular
Cytoplasm: large amount, no platelet formation
plate-producing megakaryocytes
Cytoplasm: large amount, the outer edge of the cytoplasm falls off to form platelets
naked megakaryocytes
Little or no cytoplasm
Chemical dyeing
Peroxidase POX
Mainly found in granulocytes (primordial granulocytes - enhanced with maturation reaction, basophilic -)
Neutrophil alkaline phosphatase NAP
Mainly found in the cytoplasm of mature granulocytes
clinical significance
(1) Differentiation between chronic myelogenous leukemia and leukemia-like reaction
NAP activity is significantly reduced in CML, and NAP activity is extremely increased in leukemia-like reactions.
(2) Differentiation between paroxysmal nocturnal hemoglobinuria and aplastic anemia
NAP activity decreases in the former and increases in the latter
(3) Identification of acute leukemia types
NAP activity is increased in acute lymphoblastic leukemia and decreased in acute myeloid leukemia.
(4)Other blood diseases
Lymphoma, myeloid proliferative diseases, chronic lymphocytic leukemia, etc. have moderately increased NAP activity
(5)Other situations
Adrenocortical hormone hyperfunction, pregnancy, and the use of adrenocortical hormones, estrogen, etc., may increase the NAP score
Sudan black dye SB
subtopic
Nonspecific Esterase Staining (NSE) NaF Inhibition Assay
Mainly found in monocytes, increasing with maturity
clinical significance
(1) Acute monocytic leukemia is strongly positive and can be inhibited by sodium fluoride.
(2) Both acute myeloid leukemia and acute myeloid leukemia are negative or weakly positive, but the positive reaction is not inhibited by sodium fluoride.
(3) Acute lymphocytic leukemia has a negative reaction.
Glycogen staining PAS
Reference
(1) Negative reaction of nucleated red blood cells:
2) Most lymphocytes are negative, and a few are weakly positive:
(3) In the granulocyte lineage, glycogen staining of promyelocytes is (-), and the following stages of promyelocytes are (), gradually increasing:
(4) Monocyte star weak positive reaction
(5) Positive reaction of megakaryocytes and platelet star
clinical significance
(1) Differentiate between erythroleukemia and other diseases with increased red blood cells: PAS staining is strongly positive in erythroleukemia
(2) Distinguish between benign and malignant lymphoproliferative diseases: In malignant lymphoproliferative diseases, the PSA staining integral value of lymphocytes is increased; in benign lymphocyte proliferation such as viral infection, the lymphocyte integral value is normal.
(3) Identification of three types of acute leukemia
1) In acute myeloid leukemia, PAS staining often shows negative reaction:
2) In acute lymphoblastic leukemia, the positive substances are in the form of coarse particles or lumps:
3) In acute monocytic leukemia, the positive material appears uniformly diffuse or finely granular.
iron stain
concept
(1) Extracellular iron: divided into 5 levels according to positive intensity (blue substance, blue particles, blue beads)
(2) Intracellular iron: expressed as the percentage of sideroblasts
Ring sideroblast: more than 10 thick iron granules, arranged around the nucleus for more than 2/3 of the nuclear circumference
Reference
(1) Extracellular iron: usually or
(2) Intracellular iron: the positive rate is 20-90%, with an average of 65%. 1 to 5 iron-stained granules are commonly found in the cytoplasm.
clinical significance
(1) Iron deficiency anemia: Extracellular iron is significantly reduced or disappeared, intracellular iron positivity rate is reduced, often <15%, and iron particles in the cytoplasm become smaller and lighter.
(2) Non-iron deficiency anemia: In pernicious anemia, aplastic anemia, and hemolytic anemia, the extracellular iron is mostly , and the intracellular iron positivity rate increases.
(3) Sideroblastic anemia: The intracellular iron positivity rate increases significantly, and ring sideroblasts can be seen
Acid phosphatase staining ACP
Specific esterase stain SE
Blood characteristics of common blood diseases
anemia
Classification of anemia
According to the concentration of hemoglobin
According to the shape of red blood cells
Wintrobe classification according to MCV MCHC MCH
Fuck huge bone small slow subway
Bessman classification according to MCV RDW
Aplastic anemia---uniform type
Iron deficiency and MgA solution poverty are small/large heterogeneous, respectively.
Classification according to bone marrow hyperplasia
proliferative anemia
Anemia, Iron deficiency anemia, Hemorrhagic anemia
dysplasia
AA
Ineffective hematopoiesis
MgA MDS anemia of chronic disease
According to the cause of red blood cell loss
Decreased red blood cell production
bone marrow hematopoietic dysfunction
Deficiency or utilization disorder of hematopoietic substances
Increased destruction of red blood cells
Intrinsic defects in red blood cells
External abnormalities of red blood cells
Too much red blood cell loss
Iron deficiency anemia IDA
Pathogenesis
Effects of Iron Deficiency on Iron Metabolism
Decreased iron storage indicators (ferritin, hemosiderin)
Decreased serum iron and transferrin saturation
Increased total iron binding capacity and unbound iron transferrin
Increased serum soluble transfer receptor
Iron deficiency increases free protoprin (PEP), leading to microcytic hypochromic anemia
Effects of iron deficiency on tissue and cell metabolism
Decreased activity of iron-containing enzymes and iron-dependent enzymes
clinical manifestations
Manifestations of anemia (non-specific)
Fatigue, easy fatigue, dizziness, headache, tinnitus, palpitations, shortness of breath, anorexia, paleness, increased heart rate, etc.
Manifestations of tissue iron deficiency (specific)
1. Abnormal mental behavior
Pica
2. oral cavity
Stomatitis, glossitis, lingual papilla atrophy, angular stomatitis, iron deficiency dysphagia (Plummer-Vinson syndrome), gastrointestinal disorders
3. nail
Thinning, lackluster, flattened, spatula-shaped nails (reverse nails)
4. skin hair
Dry, rough and falling off
laboratory tests
1. Blood
Microcytic hypochromic anemia, normal or slightly increased reticulocytes
2. peripheral blood smear
The red blood cells are small in size, the central light-stained area is expanded, and the ring red blood cells are increased.
3. bone marrow examination
nuclear old plasma young
Mainly erythroid hyperplasia
There were no obvious abnormalities in granulocyte and megakaryotype
Bone marrow smear iron staining: external iron is significantly reduced or disappeared, sideroblasts <15%
gold standard
4. Iron metabolism index
Serum iron (SI) ↓, serum ferritin (SF) ↓, transferrin saturation (TS) ↓
Total iron binding capacity (TIBC)↑, unbound iron transferrin↑
Ferritin is a sensitive indicator of iron stores
Megaloblastic anemiaMgA
Pathogenesis
Folic acid deficiency - DNA synthesis disorder - nuclear development stagnates, cytoplasm continues to mature - the phenomenon of "nucleo-aging" - cell division and proliferation are blocked
Atrophy of gastric mucosa leads to MgA secretion disorder of intrinsic factor (because the absorption of vitamin B requires intrinsic factor), which is called pernicious anemia
Vitamin B12 deficiency - affects sphingomyelin formation - nerve demyelination - neurological symptoms
clinical manifestations
General symptoms of anemia
special performance
Digestive system performance
Beef tongue (the surface of the tongue is as smooth as a mirror), tongue papilla atrophy, loss of appetite, nausea, bloating, diarrhea, and constipation
neuropsychiatric symptoms
Symmetrical numbness of hands and feet
laboratory tests
Blood
Mature erythrocytes vary in size, with large erythrocytes (diameter > 10 µm) being the main type. Sometimes megaloblastic erythrocytes (diameter > 15 µm), Howell-Jolly bodies, and basophilic stippling red blood cells can be seen.
The number of white blood cells is normal or reduced, and the neutrophil cell bodies are relatively large. The phenomenon of excessive lobulation of neutrophil nuclei is an early manifestation of this disease, and a few immature granulocytes are occasionally seen.
Platelet count is normal or reduced, and giant platelets may be seen
bone marrow
Active or obviously active proliferation is consistent with proliferative anemia
The ratio of granulosa to red is reduced, and the erythroid system is significantly proliferated. The granulosa system is also prone to megaloblastic changes (giant myelocytes and giant rod-shaped granulocytes are the most common), and excessively divided neutrophils and megakaryocytes can be seen.
Serum folate decreased, or both serum folate and vitamin B decreased
Other tests: Intrinsic factor blocking antibodies
Aplastic anemia (AA)
concept
It is a bone marrow dysfunction that can be caused by different causes and mechanisms. The main manifestations are low bone marrow hematopoietic function, pancytopenia, anemia, bleeding, and infection syndrome. Immunosuppressive treatment is effective.
Pathological mechanism: abnormal immune mechanism, hematopoietic stem cell defect, hematopoietic microenvironment defect
clinical manifestations
Acute aplastic anemia, sudden onset, severe symptoms
Anemia: not obvious in the early stage, obvious in the late stage
△: Aplastic anemia is progressively worse
Infections: Common in the respiratory system
fever
Bleeding: skin, mucous membranes, internal organs
△: No hepatosplenomegaly
Hepatosplenomegaly: leukemia, MM, MDS, lymphoma
laboratory tests
1. Blood routine
Pancytopenia, normocytic normochromic anemia
During treatment, platelets are the hardest to recover and red blood cells are the last to appear.
Reticulocyte count decreased, white blood cell differential showed no immature cells
△Diagnostic criteria for severe aplastic anemia (two of the following three)
1. Absolute value of reticulocytes＜15*10^9/L(0.5%)
2. Neutrophils <0.5*10^9/L
3. Platelets＜20*10^9/L
<30*10^9/L, use platelet-raising drugs
<20*10^9/L, platelet transfusion
<10*10^9/L, strict bed rest
4. If neutrophils <0.2*10^9/L, it is extremely severe aplastic anemia
2. bone marrow smear
Best diagnosis
Reduced or extremely reduced proliferation
Severe aplastic anemia: reduced proliferation in many parts, reduced bone marrow granules (compensatory increase in other parts), mainly non-hematopoietic cells; no hematopoietic cells in the bone marrow granules
Non-severe aplastic anemia: centripetal damage, with certain compensatory ability: puncture at multiple sites: significant reduction in megakaryocytes: compensatory hyperplasia of the erythroid system, dominated by highly concentrated carbon nucleoid-like late young red
3. bone marrow biopsy
Hematopoietic tissue is uniformly reduced and adipose tissue is increased
Hemolytic anemia HA
Hemolytic anemia (HA) is caused by a lack of red blood cells due to various reasons (such as cell membrane, energy metabolism enzyme and H deficiency, etc.) or abnormal external factors that shorten the life of red blood cells and accelerate their destruction, exceeding the compensatory ability of bone marrow hematopoiesis. A type of anemia caused. Excessive destruction and active proliferation coexist
Pathogenesis
Hemolysis in situ: myelodysplastic syndrome (MDS), megaloblastic anemia
intravascular hemolysis
1. PNH (paroxysmal nocturnal hemoglobinuria), cold antibody autoimmune hemolysis, favismosis
Eat some cold broad beans before going to bed
2. acute onset
3. Abnormal haptoglobin: The main function of haptoglobin is to bind to free hemoglobin to reduce hemoglobin damage to the kidneys (reduced haptoglobin is seen in intravascular hemolysis and combines with Hb to protect the kidneys)
extravascular hemolysis
Hereditary spherocytosis, thalassemia, warm antibody autoimmune hemolysis
Extraterrestrial warming
Slow onset (hemolysis in the spleen)
Classification
I. Abnormalities in red blood cells themselves
1. red blood cell membrane abnormalities
Hereditary spherocytosis, hereditary elliptocytosis, hereditary acanthocytosis, hereditary stomatocytosis
PNH
Acquired blood cell membrane glycosylated phosphoinositide (GPI) anchoring protein abnormalities
2. Abnormal red blood cell enzymes
Glucose-6-phosphate dehydrogenase deficiency (favismosis)
Anaerobic glycolytic enzyme deficiency (pyruvate kinase)
3. globin structural abnormalities
Thalassemia. sickle cell thalassemia
II. Abnormalities outside red blood cells
Autoimmune warm antibody type (IgG) or cold antibody type (IGM)
laboratory tests
Determine the existence of dissolved poverty
Excessive destruction of red blood cells
1. Increase in free HB in blood
2. Increase in serum unconjugated bilirubin
3. Urobilinogen (+) Urinary hemosiderin (+)
4. Increased serum lactate dehydrogenase activity
compensatory proliferation of red blood cells
1. Peripheral blood shows nucleated red, stippling, polychromatic red blood cells and red blood cell fragments
2. Carbo rings, H-J bodies, and reticulum counts are visible.
Contrast aplastic anemia is reduced, ineffective and iron deficiency is normal (it will increase significantly after iron deficiency treatment)
3. Erythroid hyperplasia is active and the grain-to-red ratio decreases or is inverted.
Determine the site of hemolysis
Intravascular hemolysis (acute): hb urine (soy sauce color urine), hemosiderinuria (repeated intravascular hemolysis), kidney failure, back pain, liver failure, spleen failure, jaundice
Extravascular hemolysis (slow): Goes through the spleen and liver. Hepatosplenomegaly. Freely enters the blood and combines into the gallbladder and enters the intestine. Blood free bilirubin increases and blood bileogen increases. Goes through the kidneys. Cholegenuria () Urinary bilirubin (-) Jaundice
Hemolysis in situ: MDS MDS manifestations Bilirubin
Determine the cause of hemolysis
Hereditary HA
Membrane fragility test Autohemolysis test Red blood cell enzyme defect detection Hemoglobin electrophoresis
Mainly caused by red blood cell membrane defects, enzyme defects and other self-deficiencies
Acquired HA
Antiglobulin test Acid hemolysis test Sucrose hemolysis test Cold agglutinin test Hot and cold hemolysis Flow cytometry
Mainly external defects caused by abnormal immune function
leukemia
acute leukemia
Blood
(1) Normocytic, normochromic anemia, and a few red blood cells may appear
(2) The white blood cell count may increase, decrease, or be normal, and immature cells may appear
(3) Decreased platelet count
bone marrow
(1) Bone marrow proliferation is obviously active or extremely active (other cell lines are suppressed)
(2) Excessive and abnormal proliferation of blood cells of one or two lines, with a significant increase in primitive/immature cells, ≥30% ANC
(3) Special cell shape or structure: Auer bodies, blue cells
chronic leukemia
CML
Features
Chronic onset, more common in young adults
Significant increase in granulocytes and spleen enlargement
Ph chromosome and abl/bcr fusion gene
(1) CML blood picture characteristics
1) There may be no anemia in the early stage, but normocytic anemia may occur as the disease progresses.
2) White blood cells are significantly increased, mainly neutrophils, myelocytes and promyelocytes < 10%, basophils are increased 3) Platelets are increased or normal in the early stage, and may decrease progressively in the later stage
(2) Characteristics of CML bone marrow imaging
1) Extremely active bone marrow proliferation
2) The granulocytes are significantly proliferated, and G/E is significantly increased. Cells at the mesophilic and lower stage are mainly cells, with protozoa and promyocytes <10%, and basophils and eosinophils <10%.
3) Red blood cell proliferation is inhibited
4) Megakaryocytes increase in the early stage and decrease in the late stage
CLL
Features
Elderly men, more common in Europe and America
Long course of disease
Progressive enlargement of lymph nodes throughout the body, splenomegaly
Skin lesions and immune deficiencies
(1) CLL blood picture characteristics
1) There may be no anemia in the early stage. When the disease progresses or is complicated by hemolysis, normochromic normocytic anemia may occur.
2) White blood cells increased significantly, mainly small lymphocytes
3) Neutropenia
4) Platelets may increase or be normal in the early stage, but may progressively decrease in the later stage.
(2) Characteristics of CLL bone marrow imaging
1) Bone marrow proliferation is obviously active or extremely active
2) Significant proliferation of lymphoid system, >50%, mainly mature small lymphocytes
3) The proliferation of granulosa and erythroid is inhibited, and when hemolysis occurs, erythroid can proliferate.
4) Megakaryocytes increase in the early stage and decrease in the late stage
Idiopathic thrombocytopenic purpura ITP
Features
autoimmune disease
Production of platelet antibodies, leading to excessive platelet destruction
Inhibited megakaryocyte maturation
1. Characteristics of ITP blood picture
(1) Red blood cells and hemoglobin are usually normal. Acute or chronic bleeding may be accompanied by anemia.
(2) White blood cell count is normal
(3) Thrombocytopenia
2. Characteristics of ITP bone marrow imaging
(1) Bone marrow proliferation is obviously active
(2) Proportion of erythroid and granulosa. There is usually no obvious abnormality in the shape, but the erythroid system may increase when the joint bleeds.
(3) Increased megakaryocytes and developmental disorders