Lecture on Anemias and polycythemias by Dr. Roomi

8/12/2019 Lecture on Anemias and polycythemias by Dr. Roomi

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Anemia/anaemia

• Anemia is a decrease in

number of red blood

cells (RBCs) or less than

the normal quantityof hemoglobin in the

blood.



WHO's Hemoglobin thresholds used to

define anemia





Effects of Anemia on Function of the Circulatory System/

Clinical features of Anemia

•

General symptoms: Tiredness, lassitude, easy fatiguabilityand generalized muscle weakness

• Pallor seen in skin ,nail beds & conjunctiva of eye

• Cardiovascular symptoms: – Dysponea` on exertion,

– Tachycardia (increase heart rate)

– Palpitations (subjective feeling of heart beat)

– viscosity of blood decreases,

– decreased resistance to blood flow,

– increased blood flow to the tissues, – rapid venous return to heart

– HYPERDYNAMIC circulation--- increased CO—

– increased pumping work load on heart.

–

in exercise acute cardiac failure can occur. Prolong anemia in oldpeople dilatation and failure of heart.





Aplastic Anemia

• Lack of functioning of bone marrow.

• Causes: exposure to gamma radiation(nuclear

bomb), excessive X-ray treatment, industrial

chemicals, drugs, cancer chemotherapy.

• There is decreased formation of RBCs, WBCs

(granulocytes & monocytes) & platelets.

• Pancytopenia (decrease in RBCs, WBCs and

platelets). MCQ



Blood Loss Anemia

• After acute hemorrhage: – the body replaces the fluid portion of the plasma in 1-3

days,

– but this leaves a low concentration of RBCs.

– If a 2nd hemorrhage does not occur, the RBC concentrationusually returns to normal within 3-6 wks.

• chronic blood loss: – Causes: peptic ulcers, colon cancer, endometrial caner

– a person frequently cannot absorb enough iron from theintestines to form Hb. as rapidly as it is lost.

– RBCs are then produced that are much smaller thannormal and have too little Hb inside them, giving rise tomicrocytic hypochromic anemia. MCQ









Plummer Vinson syndrome

• Spoon shape nails---

Koilonychia

• Atrophy of tongue

• Angular stomatitis(Inflammation at the

angle of mouth)

•

Difficulty in swallowing--Dysphagia



Blood picture in iron deficiency anemia

• Decrease in size of RBCs(microcytes): MCV lessthan 80 fL

• Decreased conc. Of Hb

,increased central pallorsurrounded by a rim ofHb.

• MCH & MCHC decrease(Hypochromic cells)

• Color index decreases.• Reticulocyte count

normal or decreased.











Pernicious anemia

Fish

tapeworm





Fe deficiency anemia

•

Women of poor socialeconomic status, pregnancy,lactation and infancy

• RBC count decreases

• MCHC= Decreases

• Colour Index below normal

• MCV =below 80fL(Microcytes)

• MCH = decreased,

Hypochromic

B12 deficiency anemia

•Men of middle age

• RBC Count= Decreases

• MCHC= Normal or above

normal• Color index= Above normal

• MCV= above 100 fL,

(Macrocyte)

• MCH= Remains same



Fe deficiency anemia

• Colour Index decreased

• WBCs & platelets normal

• Microcytic hypochromic

RBCs

B12 deficiency anemia

• Colour index increased

above 1.1

•Decreased,hypersegmented

neutrophilic nuclei (MCQ)

•Macrocytic normochromicRBCs



HEMOLYTIC ANEMIAS

Some examples of hemolytic anemias:

• hereditary spherocytosis

• thalassemia

• sickle-cell disease

• glucose-6-phosphate dehydrogenase deficiency

• pyruvate kinase deficiency

• autoimmune hemolytic anemia

• Lead poisoning



Thalassemias



Sickle cell Anemia

• Present in 0.3-1% of African &American blacks.

• Contains HbS whichprecipitates into crystals whenHb is exposed to low partial

pressure of O2• Hb crystals elongates the cell

& give it sickle appearance;

• Hb crystals damage the cellmembrane-hemolysis of cells-vicious cycle (sickle cell crisis)

• Cause: valine is substituted forglutamic acid at position 6 ineach of the two beta chains ofHb.





hereditary spherocytosis

• Cause: Hereditary spherocytosis is agenetic disorder caused by a varietyof molecular defects in the genesthat code for spectrin, ankyrinproteins. MCQ

• RBCs are very small and sphericalrather than being biconcave discs.

• These cells cannot withstandcompression forces because they donot have the normal loose, baglikecell membrane structure of thebiconcave discs.

• On passing through the splenic pulp

and some other tight vascular beds,they are easily ruptured by evenslight compression (increase fragilityof RBCs). MCQ



Polycythemia

• It is a disease state in which theproportion of blood volume that isoccupied by red blood cellsincreases.

• Blood volume proportions can be

measured as hematocrit level.• It can be due to an increase in the

number of red blood cells("absolutepolycythemia") or to a decrease inthe volume of plasma ("relative

polycythemia").

• The emergency treatment ofpolycythemia (e.g., in hyperviscosityor thrombosis) is removal of bloodfrom the circulation.

/ /



Primary polycythemia/ Polycythemia vera/

polycythemia rubra vera/erythremia

• Cause: It is pathological condition in which the RBCs count may be

7-8 million/mm3 and the hematocrit may be 60-70 % instead of the

normal 40-45 %. Polycythemia vera is caused by a genetic

aberration in the hemocytoblastic cells that produce the blood cells.

The blast cells no longer stop producing red cells when too manycells are already present.T his causes excess production of red blood

cells in the same manner that a breast tumor causes excess

production of a specific type of breast cell.

• Often, excess white blood cells and platelets are also produced.

• Blood volume may become double

• Blood viscosity increases from normal (3) to 10.



Secondary polycythemia

• It is caused by either natural or artificial increases inthe production of erythropoietin, hence an increasedproduction of RBCs.

• there may be 6-7 million/mm3 RBCs.

• Secondary polycythemia resolves when the underlyingcause is treated.

• physiologic secondary polycythemia: – High altitude: e.g. at 14,000-17,000 feet, where PO2 is very

low. MCQ

• pathologic secondary polycythemia: – Cardiac failure

– COPD (chronic obstructive pulmonary disease)





CYANOSIS IN POLYCYTHEMIA

Lecture on Anemias and polycythemias by Dr. Roomi

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