MTAP W3 (Hematology W14: General=Anemia) Flashcards by JHOANNA LYNN LUMBOY

derived from the greek word ‘ANAIMIA’= without blood

anemia

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decrease in number of RBCs or amount of hemoglobin in the RBCs= decreased oxygen delivery and subsequent tissue -

hypoxia

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anemia is considered to be present if the HGB and HCT is below the lower limit of the -% reference interval

95%

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RBC parameters: HGB AND HCT are affected by the individual’s -

age
gender
geographical location

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anemia arises from decrease oxygen carrying capacity of blood

it can arise if there is:
1. INSUFFICIENT hemoglobin
2. hemoglobin is NONFUNCTIONAL

which is the more frequent cause?

insufficient hemoglobin

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reduction from baseline value in total number of RBCs; hgb and rbc mass/hct

anemia

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normal or increased total red cell mass may occur with PREGNANCY, MACROGLOBULINEMIA, SPLENOMEGALY

dilutional anemia

pag may PMS=delusional

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QUANTITATIVE CHANGES IN RBCs

-decreased RBCs
-decreased oxygen carrying capacity of blood

anemia

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QUANTITATIVE CHANGES IN RBCs

-too many RBC in circulation
-increased PCV
-hypervolemia
-hyperviscosity

polycythemia vera/ erythrocytosis

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used as a screening test to evaluate if px has HEMOLYTIC ANEMIA

reticulocyte count

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normal value of hgb in women

12-15 g/dL

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normal value of hgb in men

13.5-18 g/dL

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anemia: typical of hypoproliferation

normocytic, normochromic

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CLASSIFICATION OF ANEMIA

Iron deficiency
Thalassemia
Sideroblastic anemia

low MCV, low MCHC
microcytic, hypochromic

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CLASSIFICATION OF ANEMIA

Iron deficiency
Thalassemia
Sideroblastic anemia

low MCV, low MCHC
microcytic, hypochromic

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CLASSIFICATION OF ANEMIA

Iron deficiency
Thalassemia
Sideroblastic anemia

low MCV, low MCHC
microcytic, hypochromic

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CLASSIFICATION OF ANEMIA

Bone marrow disorder
Anemia of chronic disorders
Autoimmune disease

normal MCV, normal MCHC
normocytic, normochromic

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CLASSIFICATION OF ANEMIA

Vitamin B12 deficiency
Folate deficiency
Excessive alcohol ingestion
Hypothyroidism

high MCV, normal MCHC
macrocytic, normochromic

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MECHANISM OF ANEMIA

term used for marrow erythroid proliferative activity

erythropoiesis

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MECHANISM OF ANEMIA

erythropoiesis: DEFECTIVE progenitor cells, DESTROYED in the BM before maturation

ineffective erythropoiesis

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MECHANISM OF ANEMIA

erythropoiesis: DECREASE in number of erythroid precursor cells in the BM, NOT DESTROYED

insufficient erythropoiesis

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MECHANISM OF ANEMIA

diseases associated:
1. megaloblastic anemia
2. thalassemia
3. sideroblastic anemia

ineffective erythropoiesis

‘MTS’- ineffective medtechs?

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MECHANISM OF ANEMIA

the peripheral blood HGB is low despite an increase in RBC precursors in the bone marrow

ineffective erythropoiesis

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MECHANISM OF ANEMIA

diseases associated:
infection/ parvovirus B19
sarcoidosis
acute leukemia

insufficient erythropoiesis

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CATEGORIES OF ANEMIA 1. acute 2. chronic

blood loss

CATEGORIES OF ANEMIA 1. aplastic 2. iron deficiency 3. sideroblastic anemia 4. anemia of chronic disease 5. megaloblastic

impaired production

CATEGORIES OF ANEMIA 1. inherited defects 2. acquired disorders

hemolytic

CATEGORIES OF ANEMIA Normal MCV

80-100fL

CATEGORIES OF ANEMIA Normal MCHC

31-37g/dL

CATEGORIES OF ANEMIA MORPHOLOGICAL CLASSIFICATION high MCV

macrocytic

CATEGORIES OF ANEMIA MORPHOLOGICAL CLASSIFICATION low MCV

microcytic

CATEGORIES OF ANEMIA MORPHOLOGICAL CLASSIFICATION high MCHC

hyperchromic

CATEGORIES OF ANEMIA MORPHOLOGICAL CLASSIFICATION low MCHC

hypochromic

CATEGORIES OF ANEMIA - CLASSIFICATION caused by pathophysiological mechanism responsible for the RBC deficit -decreased erythrocyte production -increased erythrocyte loss

etiologic classification

MORPHOLOGICAL CLASSIFICATION 1. bleeding 2. hypoproliferation of hematopoietic stem cells

normocytic normochromic anemia

MORPHOLOGICAL CLASSIFICATION 1.IDA 2. sideroblastic anemia

microcytic hypochromic anemia

MORPHOLOGICAL CLASSIFICATION 1. megaloblastic anemia

macrocytic normochromic anemia

2 approach for classification of anemia

1. reticulocyte count 2. MCV

signs and symptoms: NOT seen in ANEMIA

1. prone to infection 2. ruby complexion

the most important indices is the -

MCV

the least important indices is the -

MCH

tool to assess bone marrow ability to increase RBC production in response to anemia

reticulocyte count

laboratory procedures used to diagnose anemia

1. HGB 2. PLT 3. WBC 4. OFT 5. bilirubin 6. haptoglobin 'ha-bi phow'

plasma protein that binds free hemoglobin

haptoglobin

plasma protein that decreases in case of hemolytic anemia

haptoglobin

LABORATORY PROCEDURES USED TO DIAGNOSE ANEMIA increased in hemolytic anemia during lysis, found inside the RBC

LDH test

LABORATORY PROCEDURES USED TO DIAGNOSE ANEMIA reflects the body's tissue major iron stores

serum ferritin

serum ferritin in male:

12-300ng/mL

serum ferritin in female:

12-150ng/mL

LABORATORY PROCEDURES USED TO DIAGNOSE ANEMIA body's ability to transport iron, measured to identify how much iron is being carried in the blood

TIBC/ total iron binding capacity

LABORATORY PROCEDURES USED TO DIAGNOSE ANEMIA measures the total excretion of the breakdown products of heme

fecal urobilinogen

LABORATORY PROCEDURES USED TO DIAGNOSE ANEMIA determine the amount of protoporphyrin not used for hgb synthesis

FPE/ free erythrocyte protoporphyrin ZPP/ zinc protoporphyrin

LABORATORY PROCEDURES USED TO DIAGNOSE ANEMIA measured by direct-fluorescene-hematofluorometer

FEP/ free erythrocyte protoporphyrin ZPP/ zinc protoporphyrin

LABORATORY PROCEDURES USED TO DIAGNOSE ANEMIA radioactive iron is injected IV

plasma iron turnover

LABORATORY PROCEDURES USED TO DIAGNOSE ANEMIA PLASMA IRON TURNOVER rate of disappearance from blood is -hrs

2-3hrs

LABORATORY PROCEDURES USED TO DIAGNOSE ANEMIA PLASMA IRON TURNOVER 70-80% of the injected Fe appears within -days

10days

LABORATORY PROCEDURES USED TO DIAGNOSE ANEMIA uses radioactive chromium shorter life span= faster disappearance

red cell life span

INCREASED RBC CONCENTRATION HCT: higher than -L/L in male

>0.52 L/L, 52% normal value: 40-54%

INCREASED RBC CONCENTRATION HCT: higher than -L/L in female

>0.50 L/L, 50% normal value: 35-49%

are young RBCs that lack a nucleus but still contain RESIDUAL RNA

reticulocytes 2 days in BM 1 day PB

the adult reference range for reticulocyte -

0.5-1.5%

the newborn reference range for reticulocyte -

1.5-5.8%

PERIPHERAL BLOOD FILM EXAMINATION variation in shape is called

poikilocytosis

PERIPHERAL BLOOD FILM EXAMINATION variation in size is called

anisocytosis

this serves as a quality control to verify results produced by automated analyzers

peripheral blood film examination

a process that determine the M:E ratio

bone marrow examination 'slit-v' sternum, lumbar,iliac,tibia,vertebrae

bone marrow samples can be obtained by - and -

aspiration and trephine biopsy

BONE MARROW EXAMINATION - yields semi-liquid bone marrow

aspirate

BONE MARROW EXAMINATION Aspirate=semi-liquid bone marrow examined under a - microscope and analyzed by (3)

light microscope flow cytometry chromosome analysis PCR

BONE MARROW EXAMINATION frequently obtained which yields a narrow

trephine biopsy

BONE MARROW EXAMINATION trephine biopsy: examined microscopically with the aid of -

immunohistochemistry

RED CELL INDICES -liter=1 fL

10-15

RED CELL INDICES normal value of MCV

80-100fL

RED CELL INDICES MCV formula

HCT % x10/RBC

RED CELL INDICES average volume of the individual red blood cell

MCV

RED CELL INDICES average weight of hgb of the individual red cell

MCH

RED CELL INDICES normal value of MCH

27-32pg/ug

RED CELL INDICES MCH formula

HGB x10/RBC

RED CELL INDICES the percent of hgb in the average red cell

MCHC

RED CELL INDICES MCHC formula

RED CELL INDICES HGB x100/HCT%

MCV and ANEMIA CLASSIFICATION is characterized by an MCV of less than 80fL with small RBCs (<6um)

microcytic anemia

characterized by an MCHC of less tahn 32g/dL and INCREASED central pallor in the RBCs may accompany microcytosis

hypochromia

MCV and ANEMIA CLASSIFICATION is characterized by an MCV greater than 100fL with large RBCs (>8um) can be megaloblastic or non megaloblastic

macrocytic anemia

MCV and ANEMIA CLASSIFICATION caused by impaired synthesis of DNA such as Vit 12, B9/folate deficiency or myelodysplasia

megaloblasic anemia

the next test after reticulocyte count is - in classifying anemia

MCV

ARC->MCV 1. Thalassemia 2. Anemia of chronic inflammation 3. Iron deficiency 4. Lead poisoning 5. Sideroblastic anemia 6. CHronic inflammation? 7. hemoglobin E

microcytic/ low MCV

ARC->MCV 1. Aplastic anemia 2. Anemia of renal disease 3. Myelophthisic anemia 4. Infection: parvovirus B19 5. Anemia of chronic inflammation

normocytic/ normal MCV

ARC->MCV 1. Myelodyplastic syndrome 2. Aplastic anemia 3. some Drugs 4. Erythroleukemia 5. Chronic liver disease 6. Vitamin B12 deficiency 7. Folate deficiency MADEplastiC9-12

macrocytic/ high MCV

ARC: excessive RBC loss HEMOLYSIS -cause immune hemolytic anemias

EXTRINSIC causes

ARC: excessive RBC loss HEMOLYSIS -hemolytic 1. TTP 2. HUS 3. DIC

MICROangiopathic hemolytic

can help determine the cause of an anemia when used in conjunction with MCV!

RDW

CLASSIFICATION OF ANEMIA BASED ON MCV AND RDW MICROCYTIC/LOW MCV 1. Thalassemia 2. Anemia of chronic inflammation 3. Hb E disease

RDW normal/microcytic 'TAE'

CLASSIFICATION OF ANEMIA BASED ON MCV AND RDW MICROCYTIC/LOW MCV 1. Iron deficiency 2. Sickle cell thalassemia

RDW high/microcytic 'IS'

CLASSIFICATION OF ANEMIA BASED ON MCV AND RDW NORMOCYTIC/NORMAL MCV 1. Anemia of chronic inflammation 2. Anemia of renal disease 3. Acute hemorrhage 4. Hereditary spherocytosis

RDW normal/normocytic

CLASSIFICATION OF ANEMIA BASED ON MCV AND RDW NORMOCYTIC/NORMAL MCV 1. Iron, folate, Vit b12 deficiency 2. sickle cell anemia 3. Hb SC disease

RDW high/normocytic

CLASSIFICATION OF ANEMIA BASED ON MCV AND RDW MACROCYTIC/HIGHMCV 1. Aplastic anemia 2. Chronic liver disease 3. Alcoholism

RDW normal/macrocytic

CLASSIFICATION OF ANEMIA BASED ON MCV AND RDW MACROCYTIC/HIGHMCV 1. folate, B12 deficiency 2. myelodyplastic syndrome 3. chemotherapy 4. cold agglutinin 5. chronic liver dx

RDW high/macrocytic

due to defective hemoglobin synthesis resulting to cytoplasmic maturation defect

microcytic/hypochromic anemia

MICROCYTIC/HYPOCHROMIC ANEMIA type abnormalities of iron homeostasis (deficiency in metabolism)

defective heme synthesis

MICROCYTIC/HYPOCHROMIC ANEMIA DEFECTIVE HEME SYNTHESIS - anemia: commonly known as the IRON DEFICIENCY ANEMIA

sideropenic anemia

MICROCYTIC/HYPOCHROMIC ANEMIA DEFECTIVE HEME SYNTHESIS -anemia: adequate or excess iron but defective utilization. ANEMIA OF CHRONIC INFLAMMATION

sideroachrestic anemia

MICROCYTIC/HYPOCHROMIC ANEMIA DEFECTIVE HEME SYNTHESIS -anemia: defective porphyrin metabolism

sideroblastic anemia

MICROCYTIC/HYPOCHROMIC ANEMIA defective - synthesis 1. sideropenic anemia 2. sideroachrestic anemia 3. sideroblastic anemia

defective HEME synthesis

MICROCYTIC/HYPOCHROMIC ANEMIA defective - synthesis results to thalassemia and hemiglobinopathies

defective GLOBIN synthesis

MICROCYTIC/HYPOCHROMIC ANEMIA defective - synthesis deletion or mutation of globin synthesis

defective GLOBIN synthesis

MICROCYTIC/HYPOCHROMIC ANEMIA most common form of anemia

IDA

MICROCYTIC/HYPOCHROMIC ANEMIA prevalent in infants and children, pregnancy, excessive menstrual flow, elderly with poor diets, malabsorption syndromes, chronic blood loss

IDA

MICROCYTIC/HYPOCHROMIC ANEMIA clinical signs and symptoms: 1. glossitis 2. angular cheilosis 3. koilonychia 4. pica

IDA

MICROCYTIC/HYPOCHROMIC ANEMIA: IDA sore tongue

glossitis

MICROCYTIC/HYPOCHROMIC ANEMIA: IDA inflamed cracks at the corners of the mouth

angular chielosis

MICROCYTIC/HYPOCHROMIC ANEMIA: IDA spooning of the fingernails, may be seen if the deficiency is long-standing

koilonychia

MICROCYTIC/HYPOCHROMIC ANEMIA: IDA cravings for non food items such as dirt, clay, laundry starch

pica

major iron store in the body

ferritin

MICROCYTIC/HYPOCHROMIC ANEMIA: STAGES OF IDA Stage - storage depletion

stage 1

MICROCYTIC/HYPOCHROMIC ANEMIA: STAGES OF IDA Stage - transport depletion

stage 2

MICROCYTIC/HYPOCHROMIC ANEMIA: STAGES OF IDA Stage - functional depletion

stage 3

MICROCYTIC/HYPOCHROMIC ANEMIA: STAGES OF IDA Stage - HGB: normal Serum iron: normal TIBC: normal ferritin: decreased

stage 1

MICROCYTIC/HYPOCHROMIC ANEMIA: STAGES OF IDA Stage - HGB: normal Serum iron: decreased TIBC: increased ferritin: decreased

stage 2

MICROCYTIC/HYPOCHROMIC ANEMIA: STAGES OF IDA Stage - HGB: decreased Serum iron: decreased TIBC: increased ferritin: decreased

stage 3

MICROCYTIC/HYPOCHROMIC ANEMIA parasites associated with IDA (4)

1. hookworms (necator, ancylostoma) 2. T. trichiura 3. S. mansoni 4. S. haematobium

major protein that transport iron in the plasma

transferrin

MICROCYTIC/HYPOCHROMIC ANEMIA beta globulin responsible for binding iron and its transport in the blood stream

transferrin

MICROCYTIC/HYPOCHROMIC ANEMIA transferrin 1 gram can bind - mg of iron

1.25mg

MICROCYTIC/HYPOCHROMIC ANEMIA refers to the total amount of iron that transferrin can carry, capacity of transferrin to bind iron

TIBC

MICROCYTIC/HYPOCHROMIC ANEMIA an index of iron storage

% saturation

MICROCYTIC/HYPOCHROMIC ANEMIA % saturation calculated value: -

100x serum iron/TIBC

rough estimate of body iron content

ferritin

MICROCYTIC/HYPOCHROMIC ANEMIA second most common type of anemia

anemia of chronic inflammation

MICROCYTIC/HYPOCHROMIC ANEMIA Commonly associated with systemic diseases, including chronic inflammatory conditions 1. rheumatoid arthritis 2. tuberculosis 3. HIV 4. malignancies

anemia of chronic inflammation

MICROCYTIC/HYPOCHROMIC ANEMIA Due to inability to use available iron for hemoglobin production

anemia of chronic inflammation

MICROCYTIC/HYPOCHROMIC ANEMIA Impaired release of storage iron associated with increased Acute phase reactants such as Hepcidin, Ferritin and lactoferrin

anemia of chronic inflammation

MICROCYTIC/ HYPOCHROMIC ANEMIA anemia of chronic inflammation impaired release of APR such as: (3)

1. hepcidin 2. ferritin 3. lactoferrin

MICROCYTIC/ HYPOCHROMIC ANEMIA anemia of chronic inflammation impaired release of APR such as: (3)

1. hepcidin 2. ferritin 3. lactoferrin`

decreases release of iron from stores acute phase reactant / inflammation

hepcidin

- Hepcidin: Decreased Iron (because hepcidin stops iron to go outside)

increased

- Hepcidin: Increase Iron ( because iron will release)

decreased

MICROCYTIC/ HYPOCHROMIC ANEMIA -Anemia Caused by BLOCKS IN THE PROTOPORPHYRIN PATHWAY resulting in defective hemoglobin synthesis and iron overload

sideroblastic anemia

MICROCYTIC/ HYPOCHROMIC ANEMIA -Anemia Excess iron accumulates in the mitochondrial region of the immature RBC in the BM and encircles the nucleus; cells are called ringed sideroblasts (iron accumulates).

sideroblastic anemia

MICROCYTIC/ HYPOCHROMIC ANEMIA Sideroblastic Anemia EXCESS IRON ACCUMULATES in the mitochondrial region of the immature RBC in the BM and encircles the nucleus; cells are called -

ringed sideroblasts (iron accumulates)

MICROCYTIC/ HYPOCHROMIC ANEMIA Sideroblastic Anemia Excess iron accumulates in the mitochondrial region of the mature RBC in circulation ; cells are called RINGED SIDEROCYTES; inclusions are - (Pappenheimer bodies on Wright’s stained smears)

Sideroticgranules

MICROCYTIC/ HYPOCHROMIC ANEMIA Sideroblastic Anemia Siderocytes are best demonstrated using -

Perl’s Prussian blue stain

MICROCYTIC/ HYPOCHROMIC ANEMIA Sideroblastic Anemia - IRREVERSIBLE; causes of block is UNKNOWN OR IDIOPATHIC

primary

MICROCYTIC/ HYPOCHROMIC ANEMIA Sideroblastic Anemia - 1. Dimorphic 2. RARS

primary

MICROCYTIC/ HYPOCHROMIC ANEMIA Sideroblastic Anemia - REVERSIBLE; causes include alcohol, anti-TB drugs (RIFES), chloramphenicol

secondary

MICROCYTIC/ HYPOCHROMICANEMIA is most often normocytic and normochromic; however, with chronic exposure to lead, a microcytic, hypochromic clinical picture may be seen

lead poisoning

MICROCYTIC/ HYPOCHROMICANEMIA Multiple blocks in the protoporphyrin pathway that affect heme synthesis

lead poisoning

MICROCYTIC/ HYPOCHROMICANEMIA Presence of many coarse Basophilic Stippling

lead poisoning

MICROCYTIC/ HYPOCHROMICANEMIA lead poisoning will lead to acquired sideroblastic anemia and acquired porphyria

lead poisoning

MICROCYTIC/ HYPOCHROMICANEMIA It inhibits ferrochelatase and D-ALA synthase enzyme in Heme/Protoporphyrin pathway

lead poisoning

MICROCYTIC/ HYPOCHROMICANEMIA It inhibits ferrochelatase and D-ALA synthase enzyme in -

Heme/Protoporphyrin pathway

MICROCYTIC/ HYPOCHROMICANEMIA ACUTE exposure to lead: -

normocytic, normochromic

MICROCYTIC/ HYPOCHROMICANEMIA CHRONIC exposure to lead: -

microcytic, hypochromic

Serum iron and serum TIBC is -

inversely proportional

MICROCYTIC/ HYPOCHROMICANEMIA DIFFERENTIAL DIAGNOSES all are decreased increased TIBC, ZPP TZ

IDA

MICROCYTIC/ HYPOCHROMICANEMIA DIFFERENTIAL DIAGNOSES all are normal increased iron, ferritin IF

B-thalassemia

MICROCYTIC/ HYPOCHROMICANEMIA DIFFERENTIAL DIAGNOSES all are decreased increased TIBC, ferritin TF

anemia of chronic disease

MICROCYTIC/ HYPOCHROMICANEMIA DIFFERENTIAL DIAGNOSES all are increased except: decrease TIBC T

sideroblastic anemia

MACROCYTIC/ NORMOCHROMICANEMIA It is characterized by an MCV greater than -fL w/ large RBC (greater than 8 um diameter). Macrocytic anemias maybe megaloblastic or non- megaloblastic.

100fL

MACROCYTIC/ NORMOCHROMICANEMIA The most common causesof megaloblastic anemia are acquired, although congenital forms exist. Deficiencies in -,-, or both account for the majority of cases

cobalamin (B12) folate (B9)

Red blood cells in megaloblastic anemias have an abnormal nuclear maturation and imbalance between nuclear and cytoplasmic maturation

MACROCYTIC/ NORMOCHROMICANEMIA

Refers to the abnormal marrow erythrocyte precursor seen in processes, such as pernicious anemia, associated with altered DNA synthesis.

MACROCYTIC/ NORMOCHROMICANEMIA

CLASSIFICATION BASED ON MCV MACROCYTIC/MCV - 1. Aplastic anemia 2. Chronic liver disease 3. Alcoholism

nonmegaloblastic

CLASSIFICATION BASED ON MCV MACROCYTIC/MCV - 1. B12 deficiency 2. B9 deficiency 3. Myelodysplasia 4. Erythroleukemia 5. Drugs

megaloblastic

CLASSIFICATION BASED ON MCV NORMOCYTIC/MCV Reticulocytes: INCREASED= hemolytic anemia - 1. membrane defects 2. hemoglobinopathies 3. enzyme deficiencies

intrinsic

CLASSIFICATION BASED ON MCV MACROCYTIC/MCV Reticulocytes: - 1. aplastic anemia 2. anemia of renal dx 3. myelophthisic anemia 4. infection; parvovirus B19 5. anemia of chronic inflammation

normal or decreased

MACROCYTIC/ NORMOCHROMICANEMIA disruption of cholesterol-to-phospholipid ratio NO IMPAIRMENT of DNA synthesis ROUND NO HYPERSEGMENTED

non-megaloblastic anemia

MACROCYTIC/ NORMOCHROMICANEMIA IMPAIRED DNA synthesis OVAL HYPERSEGMENTED

megaloblastic anemia

MACROCYTIC/ NORMOCHROMICANEMIA - ANEMIA 1. B12 deficiency 2. B9 deficiency 3. acute erythroleukemia 4. myelodysplasia 5. congenital dyserythropoietic anemia type 1 and 3

megaloblastic anemia

MACROCYTIC/ NORMOCHROMICANEMIA Defective DNA synthesis causes abnormal nuclear maturation; RNA synthesis is normal, so the cytoplasm is not affected. The nucleus matures slower than the cytoplasm (Asynchronism)

megaloblastic anemia

MACROCYTIC/ NORMOCHROMICANEMIA Laboratory picture of Pancytopenia,Oval macrocyte, Howell-jolly bodies, Hypersegmentedneutrophil

megaloblastic anemia

MACROCYTIC/ NORMOCHROMICANEMIA defect in - affects cytoplasm

RNA

MACROCYTIC/ NORMOCHROMICANEMIA defect in - affects nucleus

DNA

SCREENINGTEST USED TO DIAGNOSE MEGALOBLASTIC ANEMIA (5)

1. CBC 2. Reticulocyte count 3. WBC differential 4. bilirubin 5. LDH

SCREENINGTEST USED TO DIAGNOSE MEGALOBLASTIC ANEMIA macrocytes, pancytopenia

CBC

SCREENINGTEST USED TO DIAGNOSE MEGALOBLASTIC ANEMIA Decreased: megaloblastic anemia

reticulocyte count

MACROCYTIC/ NORMOCHROMICANEMIA VITAMIN B12 (COBALAMIN)DEFICIENCY -anemia: –caused by deficiency of INTRINSIC FACTOR, Antibody to intrinsic factor or antibodies to parietal cells, autoimmune disease.

pernicious anemia

MACROCYTIC/ NORMOCHROMICANEMIA VITAMIN B12 (COBALAMIN)DEFICIENCY parasite that causes cobalamin deficiency

D. latum

takes 3-6 years to develop because of high body stores Clinical symptoms: Jaundice, weakness, glossitis,GIbleeding, numbness and CNSPROBLEMS

pernicious anemia

Vitamin B12 intrinsic factor is needed for its proper absorption in the - intrinsic factor is produced in the PARIETAL cells

ileum

regulates the folate synthesis (DNA)

Vitamin B12

MACROCYTIC/ NORMOCHROMICANEMIA FOLIC ACIDDEFICIENCY Associated with poor diet, pregnancy or chemotherapeutic anti folic drugs such as -

METHOTREXATE

MACROCYTIC/ NORMOCHROMICANEMIA Clinical symptoms: same with vitamin B12deficiency, except NO CNSinvolvement

folic acid deficiency

other name of folic acid

Pteroylmonoglutamic acid

Vitamin B9/folic acid absorbed in -

jejunum

MACROCYTIC/ NORMOCHROMICANEMIA Acts asco-enzyme in the formation of thymidylate synthetase

FolicAcid (Pteroylmonoglutamic acid)

MACROCYTIC/ NORMOCHROMICANEMIA Thymidylate synthetase –needed to produce thymidine (one of the pyrimidine basesofDNA)

FolicAcid (Pteroylmonoglutamic acid)

MACROCYTIC/ NORMOCHROMICANEMIA Dietary aspects: B-: meat

B12

MACROCYTIC/ NORMOCHROMICANEMIA Dietary aspects: B-: vegetables

CAUSESOFFOLICACIDDEFICIENCY - is acondition that DAMAGES THE LINING OF THE SMALL INTESTINE and prevents it from absorbing parts of food that are important for staying healthy

Celiac disease

CAUSESOFFOLICACIDDEFICIENCY - is a MALABSORPTION disease commonly found in the tropical regions, marked with ABNORMAL FLATTENING OF THE VILLI AND INFLAMMATION of the lining of the SMALL INTESTINE

tropical sprue

MACROCYTIC/ NORMOCHROMICANEMIA *Include Alcoholism, Liver disease, and conditions causes accelerated erythropoiesis * RBC are ROUND not oval

NON- MEGALOBLASTICANEMIA

MACROCYTIC/ NORMOCHROMICANEMIA IMPORTANT FINDINGS IN MEGALOBLASTIC ANEMIA (5)

1. ineffective erythropoiesis and decreased retics,wbc,platelets 2. hypersegmented neutrophils 3. macroovalocytes 4. howell-jolly bodies

anemia is characterized by an MCV in the range of 80 to 100 fL.

normocytic

- anemia a DIMORPHIC POPULATION OF MICROCYTES AND MACROCYTES that can yield a normal MCV

Normocytic-Normochromic Anemia

NORMOCYTIC-NORMOCHROMIC ANEMIA - anemia Bone marrow failure causes PANCYTOPENIA (decrease of blood cells).

aplastic anemia

NORMOCYTIC-NORMOCHROMIC ANEMIA - anemia poor prognosis with complications that include bleeding, infection, and iron overload due to frequent transfusion needs.

aplastic anemia

NORMOCYTIC-NORMOCHROMIC ANEMIA - anemia 15-20% of cases 1.fanconi anemia 2. dyskeratosis congenita 3. shwachmann-bodian-diamond syndrome

INHERITED aplastic anemia

NORMOCYTIC-NORMOCHROMIC ANEMIA - anemia 80-85% of cases 1.idiopathic 2. secondary

ACQUIRED aplastic anemia

NORMOCYTIC-NORMOCHROMIC ANEMIA - anemia most common aplastic anemia

ACQUIRED aplastic anemia

ANORMOCYTIC-NORMOCHROMIC ANEMIA - ACQUIRED aplastic anemia 50-70% DIAMOND BLACKFAN ANEMIA

idiopathic/ unknown cause

ANORMOCYTIC-NORMOCHROMIC ANEMIA ACQUIRED aplastic anemia 10-75% (exposure to drugs such as sulfonamides and chloramphenicol) , chemicals (benzene), radiation or infection)

secondary

A NORMOCYTIC-NORMOCHROMIC ANEMIA problem -: microcytic

heme

A NORMOCYTIC-NORMOCHROMIC ANEMIA problem -: macrocytic

nucleus

A NORMOCYTIC-NORMOCHROMIC ANEMIA - anemia Autosomal recessive trait Dwarfism, renal disease, mental retardation

A NORMOCYTIC-NORMOCHROMIC ANEMIA - anemia Strong association with malignancy development, especially ACUTE LYMPHOBLASTIC LEUKEMIA

Genetic aplastic anemia Fanconi anemia

Acquired aplastic anemia (secondary) caused by: Antibiotics: (2)

1.chloramphenicol 2. sulfonamides

Acquired aplastic anemia (secondary) caused by: Chemicals: (2)

1. benzene 2. herbicides

NORMOCYTIC-NORMOCHROMIC ANEMIA About 30% of acquired aplastic anemias are due to drug exposure.

Acquired aplastic anemia (secondary)

NORMOCYTIC-NORMOCHROMIC ANEMIA low RBCs, normal WBC and PLT

Diamond-Blackfan anemia

NORMOCYTIC-NORMOCHROMIC ANEMIA -anemia Hypoproliferative anemia caused by replacement of bone marrow hematopoietic cells by malignant cells or fibrotic tissue

myelophthisic (marrow replacement) anemia

NORMOCYTIC-NORMOCHROMIC ANEMIA -anemia Associated with cancers (breast, prostate, lung, melanoma) with bone metastasis

myelophthisic (marrow replacement) anemia

NORMOCYTIC-NORMOCHROMIC ANEMIA -anemia Laboratory: Normocytic/normochromic anemia; leucoerythroblastic blood picture (high WBC and high immature RBC)

myelophthisic (marrow replacement) anemia

NORMOCYTIC-NORMOCHROMIC ANEMIA -anemia Characterized by a sudden loss of blood resulting from trauma or other severe forms of injury

acute blood loss anemia

NORMOCYTIC-NORMOCHROMIC ANEMIA -anemia Clinical symptoms: Hypovolemia, rapid pulse, low blood pressure, pallor

acute blood loss anemia

NORMOCYTIC-NORMOCHROMIC ANEMIA -anemia Initially normal reticulocyte count hemoglobin/ hematocrit; in a few hours, increase in platelet count and LEUKOCYTOSIS with a LEFT SHIFT, drop in hemoglobin/ hematocrit and RBC

acute blood loss anemia

reticulocytosis in - days

3-5 days

NORMOCYTIC-NORMOCHROMIC ANEMIA shift to the -: immature WBC

left

NORMOCYTIC-NORMOCHROMIC ANEMIA shift to the -: hypersegmented cells

right

NORMOCYTIC-NORMOCHROMIC ANEMIA - anemia Characterized by a gradual, lLON-TERM loss of blood; often caused by gastrointestinal bleeding

NORMOCYTIC-NORMOCHROMIC ANEMIA - anemia Initially normocytic/normochromic anemia that over time causes a DECREASE in hemoglobin/hematocrit; gradual loss of iron causes microcytic/hypochromic anemia

NORMOCYTIC-NORMOCHROMIC ANEMIA - anemia due to - All cause a normocytic/normochromic anemia; usually hereditary with INCREASE reticulocytosis due to accelerated destruction

hemolytic anemias due to intrinsic defects

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS - DEFECT 1. Hereditary spherocytosis 2. Hereditary elliptocytosis (ovalocytosis) 3. Hereditary stomatocytosis 4. Hereditary acanthocytosis (abetalipoproteinemia)

membrane defects

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS - DEFECT 1. G6PD deficiency 2. PK deficiency 3. Paroxysmal nocturnal hemoglobinuria/ PNH

enzyme defects

one altered copy of a gene is enough to cause a disease

autosomal dominant= hereditary spherocytosis

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS MEMBRANE DEFECT MOST COMMON membrane defect; autosomal dominant

hereditary spherocytosis

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS MEMBRANE DEFECT characterized by splenomegaly, variable degree of anemia, spherocytes on the peripheral blood smear

hereditary spherocytosis

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS MEMBRANE DEFECT Increased permeability of the membrane to sodium Results in loss of membrane fragments; erythrocytes have DECREASED surface area-to-volume ratio; rigid spherocytes culled/removed by splenic macrophages

hereditary spherocytosis

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS MEMBRANE DEFECT Laboratory: 1. MCHC may be >37 g/dL, increased 2. osmotic fragility 3. increased serum bilirubin

hereditary spherocytosis

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS MEMBRANE DEFECT Autosomal dominant; most persons asymptomatic due to normal erythrocyte life span; >25% ovalocytes on the peripheral blood smear

hereditary ovalocytosis

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS MEMBRANE DEFECT Membrane defect is caused by POLARIZATION OF CHOLESTEROL at the ends of the cell rather than around pallor area.

hereditary ovalocytosis

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS MEMBRANE DEFECT Autosomal dominant; variable degree of anemia; up to 50% stomatocytes on the blood smear.

Hereditary stomatocytosis

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS MEMBRANE DEFECT Membrane defect due to abnormal permeability to both SODIUM AND POTASSIUM; causes erythrocyte swelling

Hereditary stomatocytosis

both altered copies of the gene are needed to cause the dx

autosomal recessive

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS MEMBRANE DEFECT Autosomal recessive; mild anemia associated with steatorrhea, neurological and retinal abnormalities; 50- 100% of erythrocytes are acanthocytes

Hereditary acanthocytosis (abetalipoproteinemia)

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS MEMBRANE DEFECT Increased cholesterol:lecithin ratio in the membrane due to abnormal plasma lipid concentrations; absence of serum p-lipoprotein needed for lipid transport

Hereditary acanthocytosis (abetalipoproteinemia)

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS ENZYME DEFECT SEX-linked enzyme defect; most common enzyme deficiency in the HEXOSE MONOPHOSPHATE SHUNT

G6PD (glucose-6-phosphate dehydrogenase) deficiency

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS ENZYME DEFECT Reduced glutathione levels are not maintained because of decreased NADPH generation.

G6PD (glucose-6-phosphate dehydrogenase) deficiency

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS ENZYME DEFECT Results in oxidation of hemoglobin to methemoglobin (Fe3+); denatures to form HEINZ BODIES

G6PD (glucose-6-phosphate dehydrogenase) deficiency

pathway that produces glutathione

hexose monophosphate shunt

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS ENZYME DEFECT Autosomal recessive; most common enzyme deficiency in EMBDEN-MEYERHOF PATHWAY

Pyruvate kinase (PK) deficiency

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS ENZYME DEFECT Severe hemolytic anemia with reticulocytosis and echinocytes

Pyruvate kinase (PK) deficiency

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS ENZYME DEFECT An acquired membrane defect in which the red cell membrane has an increased sensitivity for complement binding as compared to normal erythrocytes

Paroxysmal nocturnal hemoglobinuria (PNH)

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS ENZYME DEFECT decrease of cd55 and cd59 All cells are abnormally sensitive to lysis by complement

Paroxysmal nocturnal hemoglobinuria (PNH)

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIAS DUE TO INTRINSIC DEFECTS ENZYME DEFECT Characterized by pancytopenia uses Ham's and sugar water test

Paroxysmal nocturnal hemoglobinuria (PNH)

Hams and sugar water test have been tradiotionally used in diagnosis of PNH the standard now used is - to detect CD 55, CD 59

flowcytometry

decreased CD59 means

MRL/ membrane inhibitor of reactive lysis

decreased CD55 means

DAF/ decay accelerating factor

NORMOCYTIC-NORMOCHROMIC ANEMIA - anemia due to - All cause a normocytic/normochromic anemia due to defects extrinsic to the RBC. All are acquired disorders that cause accelerated destruction with reticulocytosis.

Hemolytic Anemias Due to Extrinsic/Immune Defects

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIA DUE TO - DEFECTS 1. Warm autoimmune hemolytic anemia (WAIHA) 2. Cold autoimmune hemolytic anemia (CAIHA or cold hemagglutinin disease) 3.Paroxysmal cold hemoglobinuria (PCH) (extrinsic) 4.Hemolytic transfusion reaction 5. Hemolytic disease of the newborn (HDN)

hemolytic anemia due to extrinsic/immune defects

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIA DUE TO - DEFECTS Paroxysmal cold hemoglobinuria/PCH

extrinsic

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIA DUE TO IMMUNE DEFECTS - anemia RBCs are coated with IgG and/or complement. Macrophages may phagocytize these RBCs, or they may remove the antibody or complement from the RBC's surface, causing membrane loss and spherocytes.

Warm autoimmune hemolytic anemia (WAIHA)

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIA DUE TO IMMUNE DEFECTS - anemia 60% of cases are IDIOPATHIC; other cases are secondary to diseases that alter the immune response (e.g., chronic lymphocytic leukemia, lymphoma); can also be drug induced.

Warm autoimmune hemolytic anemia (WAIHA)

IgG and complement react to -c WITH LYSIS

37c/BT

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIA DUE TO IMMUNE DEFECTS - anemia Laboratory Findings 1. Spherocytes 2. MCHC may be >37 g/dL 3. Increased osmotic fragility, bilirubin, reticulocyte count 4. Occasional nRBCs present 5. Positive direct antiglobulin test (DAT) helpful in differentiating from hereditary spherocytosis

Warm autoimmune hemolytic anemia (WAIHA)

DAT (direct antihuman globulin test) (+)

WAIHA

DAT (direct antihuman globulin test) (-)

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIA DUE TO IMMUNE DEFECTS - anemia RBCs are coated with IgM and complement at temperatures below 37°C. RBCs are lysed by complement or phagocytized by macrophages. Antibody is usually anti-I but can be anti-i.

Cold autoimmune hemolytic anemia (CAIHA or cold hemagglutinin disease)

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIA DUE TO IMMUNE DEFECTS - anemia Can be idiopathic, or secondary to Mycoplasma pneumoniae, lymphoma, or infectious mononucleosis If antibody titer is high enough, sample must be warmed to 37°C to obtain accurate RBC and indices results.

Cold autoimmune hemolytic anemia (CAIHA or cold hemagglutinin disease)

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIA DUE TO IMMUNE DEFECTS - anemia Laboratory Findings: Seasonal symptoms RBC clumping can be seen both macroscopically and microscopically MCHC >37 g/dL Increased bilirubin and reticulocyte count Positive DAT detects complement-coated RBCs

CAIHA

IgM and complement reacts at -c NO LYSIS

4c/ ref temp

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIA DUE TO IMMUNE DEFECTS - anemia An IgG biphasic Donath-Landsteiner antibody with P specificity fixes complement to RBCs in the cold (less than 20°C); the complement-coated RBCs lyse when warmed to 37°C.

Paroxysmal cold hemoglobinuria (PCH)

NORMOCYTIC-NORMOCHROMIC ANEMIA HEMOLYTIC ANEMIA DUE TO IMMUNE DEFECTS - anemia Laboratory Findings: Variable anemia following hemolytic process Increased bilirubin and plasma hemoglobin Decreased haptoglobin DAT may be positive Donath-Landsteiner test positive

Paroxysmal cold hemoglobinuria (PCH)