Top Banner
RBC Morphology I. RBC Size II. Hemoglobin Content III. RBC shape ken myer abansi
43
Welcome message from author
This document is posted to help you gain knowledge. Please leave a comment to let me know what you think about it! Share it to your friends and learn new things together.
Transcript
Page 1: Hematology signed

RBC Morphology

I. RBC SizeII. Hemoglobin ContentIII. RBC shape

ken myer abansi

Page 2: Hematology signed

RBC Morphology RBC SizeNormal size is 6-8 u in diameter (NORMOCYTIC RBC/ NORMAL RBC)*******************************************ANISOCYTOSIS

→variation in RBC size●Normocytic ●Microcytic : < 6 u●Macrocytic : > 8 u; appear as large, mature RBC●Megalocytic : > 10u -12u

KEN MYER ABANSI

Page 3: Hematology signed

Clinical Significance (MACROCYTIC)

●Caused by increase erythropoietin stimulation, increase synthesis of hgb●Due to Vit. B12 and folic acid deficiency●Cirrhosis●Hemolytic anemia●Pernicious anemia

KEN MYER ABANSI

Page 4: Hematology signed

Clinical Significance (MiCROCYTE)●Caused by impaired globulin synthesis●Decreased hgb synthesis●Mitochondrial abnormality, affecting synthesis of heme●Deficiency of iron and other building materials●Failure of cell division or polyploidy (kaya malaki)

Page 5: Hematology signed

Clinical Significance (Megalocyte)

●Due to Vit B12 and folic acid deficiency●Failure of cell division or polyploidy (the reason why it's big)●Megaloblastic anemia

Page 6: Hematology signed

RBC Morphology HGB content

Normal: Central pallor occupies about 1/3 the size of the RBC (NORMOCHROMIC)*******************************************ANISOCHROMATASIA

→variation in staining property of hgb●Hypochromic : increased central pallor●Hyperchromic: no central pallor●Anulocyte : only periphery unstains hgb

Page 7: Hematology signed

RBC Morphology HGB content

●Hyperchromic/Hyperchromasia/Hyperchromia

→entire cells stain deep pink and lacks central pallor

→Clin.Sig. (does not represent true situation, suggestive of:)

● Megalocytes of pernicious anemia● Blood poisoning● Acute leukemias

Page 8: Hematology signed

RBC Morphology HGB content●Polychromatophilia/Polychromasia→ cytoplasm of non nucleated RBCs have a grayish

blue tint →Basophilic material gives a diffuse homogenous blue

color →property of rreticulocytes when stained with

Wright's →Clin. Sig.:

● Associated with rapid RBC regeneration and increase bone marrow activity

● Reticulocytosis● Pernicous anemia● Leukemia● malaria

Page 9: Hematology signed

RBC Morphology HGB content● Target cells

→other names are

– Leptocyte

– Platycyte

– Mexican hat

– Bull's eye

– Codocyte

● RBCs show hgb conc. At the outer rim and center

● A pale circular zone separates the 2 areas

● Clin.Sig.– Hemoglobinopathies– Liver disorders– Iron deficiencies– Hgb C dse– After splenectomy

Page 10: Hematology signed

RBC Morphology HGB content

● Anulocyte →Thin Rbc that are poorly hemoglobinized and

exhibit a thin peripheral ring stained hgb

● Clin.Sig.

– Hemoglobinopathies

Page 11: Hematology signed

Inclusion Bodies →a normal RBC has no inclusion bodies

→RBC must be anucleated

● ARTIFACTS

→refractile areas and crenation in the RBCs

→clinical sig.

– Water in wright's stain

– Poor staining technique

– Insufficient drying of slide prior to staining

Page 12: Hematology signed

Inclusion Bodies● BASOPHILIC STIPPLING

→coarse granulation resulting from RNA aggregates

→clinical sig.

– Non specific anemias

– Lead intoxication

Page 13: Hematology signed

Inclusion Bodies● CABOT RINGS

→thread like, round, oval, or figure of 8 loops

→due to residual nuclear membrane

→clinical sig.

– Pernicous anemia

– Lead intoxication

Page 14: Hematology signed

Inclusion Bodies● HEINZ BODIES→dark staining, round areas resulting from precipitated denatured hgb

→bind to the red cell membrane and alter its rigidity , resulting in premature destruction in the spleen

→the spleen also removes membrane bound Heinz bodies from red cells resulting in “blister “ or “bite” cells

→clinical sig.

– G-6-PO4 defficiency

– Heinz body anemias

KEN MYER ABANSI

Page 15: Hematology signed

Inclusion Bodies● HOWELL JOLLY BODIES

→eccentric, small, round, non refractile purple masses consisting of DNA nuclear remnant

→clinical sig.

– Hemolytic anemia

– Post splenectomy

Number 3s

Page 16: Hematology signed

Inclusion Bodies● HGB C CRYSTALS

→oblong, hexagonal in shape resulting from hgb found in cytoplasm of RBC

→The “washington monument” or octahedral appaerance is typical, with a clear area around the crystal. These crystals may also be shaped like a rod, spherocytic, rhomboid, or hexagon

→clinical sig.

– Hgb C disease : mild hemolytic anemia with splenomegaly that is often aymptomatic but may result in jaundice and abdominal discomfort

– Hgb SC dse

Page 17: Hematology signed

Inclusion Bodies● PARASITES

→most common

→variable appearance depending on the parasite

→clinical sig.

– Plasmodium infection

– Babesia infection

Page 18: Hematology signed

Inclusion Bodies● PAPPENHEIMER BODIES/ SIDEROTIC

GRANULES

→small, blue granules usually appearing in clusters near the periphery of RBC

→consists of non-iron heme

→clinical sig.

– Post splenectomy

– Sideroblastic anemia

– Sickle cell anemia

Page 19: Hematology signed

RBC Morphology RBC shape● ACANTHOCYTES

→Other names

– Thorn cell(acanthol)

– Spur cell

– Spike cell

→spherical, irregularly spaced spinous processes; some have bent tip due to membrane defect

→characterized by a progressive increase in sphingomyelin- lecithin ratio

→clinical sig.

– Abetalipoproteinemia

– Hemolytic anemia

– Neonatal hepatitis

– Liver disorders

Page 20: Hematology signed

RBC Morphology RBC shape● BLISTER CELL

→contains single or multiple vacuoles on markedly thinned areas at the periphery

→characterized by a progressive increase in sphingomyelin- lecithin ratio

→clinical sig.

– Presence results from trauma as cells pass through involved blood vessels

Page 21: Hematology signed

RBC Morphology RBC shape● BURR CELLS

→RBCs have uniformly spaced pointed projections on their outer edges

→clinical sig.

– Uremia

– Acute blood loss

– Cancer of the stomach

– Pyruvate kinase deficiency

Page 22: Hematology signed

RBC Morphology RBC shape

● CRENATED RBCs→also known as Echinocyte (from Gk. Word echinos = sea urchin)

→wrinkled, serrated periphery, uniform projections, uniformly spaced bumps

→blunt spicules

→clinical sig.

– Faulty drying

– Not clinically diagnostic

– Due to dehydration, hypertonic agents,and lytic agents

– Due to exposure to anticoaguants

Page 23: Hematology signed

RBC Morphology RBC shape

● DACROCYTES/ TEARDROP CELLS

→fr. Gk. Word Darkry = tear

→clinical sig.

– Severe anemias

– myelofibrosis

Page 24: Hematology signed

RBC Morphology RBC shape

● ELLIPTOCYES/ OVALOCYTES

→has bipolar aggregates of hgb that cause the cell to be slightly to severely elongated instead of biconcave

→clinical sig.

– Hereditary elliptocytes

– Thalassemia

– Sickle cell anemia

Page 25: Hematology signed

RBC Morphology RBC shape

● KERATOCYTE

→aka Helmet cell

→irregularly contracted , triangular cells

→remnants of ruptured blister cell →clinical sig.

– DIC (disseminated intravascular coagulation)

– Microangiopathic anemia

Page 26: Hematology signed

RBC Morphology RBC shape

● KNIZOCYTE/ TRIANGLE CELLS

● →RBCs looked pinched into a triangular shape

→clinical sig.

– Hemolytic anemia

Page 27: Hematology signed

RBC Morphology RBC shape

● PYKNOCYTES

→distorted, contracted RBC similar to Burr cells

→clinical sig.

– Seen in the first 2-3 months of life

– G-6-PO4 deficiency

– Microangopathic anemia

– Hemolytic anemia

KEN MYER ABANSI

Page 28: Hematology signed

RBC Morphology RBC shape● SICKLE CELLS

→ aka Drepanocytes, Menisocytes

→Elongated, slightly curved cells with pointed ends

→center of cell contains a dense crystalline area of hgb that fades somewhat towards the periphery

→clinical sig.

– Associated with hgbs in sickle cell anemia (sca)

Page 29: Hematology signed

RBC Morphology RBC shape

● SPHEROCYTES

→spherical, non-biconcave (lack central pallor)

→have dark stained center instead of the normal central pallor

→smaller surface area than the cell size; characterized by increase osmotic fragility

→clinical sig.

– Hemolytic anemia

– HDN

– Hereditary spherocytosis (most common)

Page 30: Hematology signed

RBC Morphology RBC shape

● STOMATOCYTE

→stoma or mouth aka Mouth / Stoma cell

→shows oval or rectangular (slit-like) area of central pallor

→clinical sig.– Liver disease

– Electrolyte imbalance

– Hereditary

stomatocytosis

– artifacts

Page 31: Hematology signed

RBC Morphology RBC shape

● SCHISTOCYTE

→SCHIS - cut

→fragmented RBC; a piece of the RBC is missing causing the reultant RBC to appear; fragmented/ distorted

→clinical sig.

– DIC (disseminated intravascular coagulation)

– Mecahnical trauma (most common)

Page 32: Hematology signed

Miscellaneous● Rouleaux Formation

→RBCs stack together like a roll of coins

→Saline will disperse Rouleaux

→clinical sig.

– Caused by increased CHON (most common)

– Multiple myeloma

– Waldenstrom's macroglobulinemia

Page 33: Hematology signed

Miscellaneous● Agglutination

→Disorderly clumping of RBC →clinical sig.

– RBC antibodies

– autoagglutinins

Page 34: Hematology signed

Miscellaneous● Giant pit

→Round purple bodies

→longer than normal pit but smaller than lymphocyte

→clinical sig.

– none

Page 35: Hematology signed

Qualitative Disorders of Granulocytes● Dohle Bodies

→smear reveals pale blue staining area within the neutrophil cytoplasm

→irregularly shaped blue staining area in the cytoplasm due to free ribosomes or RER

→seen with infections →clinical sig.

– Bacteria infection

Page 36: Hematology signed

Qualitative Disorders of Granulocytes● Pyknotic nucleus

● →smear reveals neutophils with condensed round nuclei or nuclear fragments

→clinical sig.

– Bacterial infection

– Prolonged contact of neutrophils with EDTA

Page 37: Hematology signed

Qualitative Disorders of Granulocytes● Toxic granulation

→smear reveals small dark staining granules within the cytoplasm of neutrophils

→increased number and prominence of the azurophilic (primary) granules

→seen most often with bacterial infections and in association with cytoplasmic vacuolization

→clinical sig.

– Bacteria infection

– Neutrophils induced to increased production of primary granules containing lysozymes

Page 38: Hematology signed

Qualitative Disorders of Granulocytes● Toxic vacuoles

→smear reveals holes in the cytoplasm of neutrophils

→blister cell counterpart sa RBC →clinical sig.

– Bacteria infection

– As bacteria are digested by neutrophils , its vacuoles appear in the cytoplasm

– Due to prolonged EDTA contact

Page 39: Hematology signed

Qualitative Disorders of Granulocytes● Lupus Erythematosus cell

→smear reveals neutrophils that have engulfed homogenous nuclear masses

→as a result, the nucleus of the neutrophils are pushed to the periphery of the cell

→the phagocytized nucleus occupies most of the cytoplasm area

KEN MYER ABANSI

Page 40: Hematology signed

Qualitative Disorders of Granulocytes● Hypersegmentation

● →polymorphonuclear leaukocyte normally have 3 or 4 lobes but 5/6 or more lobes indicate hypersegmentation

→clinical sig.

– seen most often with megaloblastic anemia , sometimes with myeloproliferative disorders

– ff. Chemotherapy (particularly metho trexate chemotherapy)

Page 41: Hematology signed

Qualitative Disorders of Granulocytes● Smudge cell / Basket Cell

→a ruptured cell remnant , classically associated with fragile lymphocyte, in CLL

Page 42: Hematology signed

Qualitative Disorders of Granulocytes● Pelger-Huet anomaly

→an autosomal dominant condition with neutrophils that are mostly bilobed in the heterozygote (normal fxn ) and unilobate in the homozygote (fatal)

Page 43: Hematology signed

Qualitative Disorders of Granulocytes● May-Hegglin anomaly

→rare disorder with large prominent Dohle like bodies

● Chediak-Higashi syndrome

→rare disorder with large neutrophilic granules representing abnormal lysosomes

KEN MYER ABANSI