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Anemia/anaemia

Anemia is a decrease in number of red blood

cells (RBCs) or less than the normal quantity

of hemoglobin in the

blood.

Anemia/anaemia • Anemia is a decrease in number of red blood cells (RBCs) or less than

WHO's Hemoglobin thresholds used to

define anemia

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 fatiguability and 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 COincreased pumping work load on heart.

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

Effects of Anemia on Function of the Circulatory System/ Clinical features of Anemia

CNS symptoms:

Fainting, Headache, spots before the eyes, lack of concentration, drowsiness, numbness, clouding of consciousness.

Reproductive system:

Amennorrhea (lack of menses)

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 2 nd hemorrhage does not occur, the RBC concentration usually 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 the intestines to form Hb. as rapidly as it is lost.

RBCs are then produced that are much smaller than normal and have too little Hb inside them, giving rise to microcytic 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

Plummer Vinson syndrome • Spoon shape nails--- Koilonychia • Atrophy of tongue • Angular stomatitis (Inflammation

Blood picture in iron deficiency anemia

Decrease in size of RBCs (microcytes): MCV less than 80 fL

Decreased conc. Of Hb ,increased central pallor surrounded by a rim of Hb.

MCH & MCHC decrease

(Hypochromic cells)

Color index decreases.

Reticulocyte count normal or decreased.

Blood picture in iron deficiency anemia • Decrease in size of RBCs ( microcytes ): MCV

Megaloblastic Anemia

Loss of vitamin B12,

folic acid, and intrinsic

factor from the stomach mucosa can lead to slow reproduction of

erythroblasts in the

bone marrow.

As a result, the red cells

grow too large, with odd shapes, and are called megaloblasts.

Megaloblastic Anemia • Loss of vitamin B12, folic acid, and intrinsic factor from the stomach mucosa

Pernicious anemia

Fish

tapeworm

Fe deficiency anemia

B12 deficiency anemia

Women of poor social economic status, pregnancy,

lactation and infancy

RBC count decreases

MCHC= Decreases

Colour Index below normal

MCV =below 80fL

(Microcytes)

MCH = decreased, Hypochromic

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 normochromic RBCs

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 which precipitates into crystals when Hb is exposed to low partial pressure of O2

Hb crystals elongates the cell

& give it sickle appearance;

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

Cause: valine is substituted for glutamic acid at position 6 in each of the two beta chains of Hb.

Sickle cell Anemia • Present in 0.3-1% of African & American blacks. • Contains HbS which
Sickle cell Anemia • Present in 0.3-1% of African & American blacks. • Contains HbS which

Erythroblastosis Fetalis

Rh+ve RBCs in fetus are

attacked by IgG antibodies by Rh ve mother.

The Rh+ve cells of fetus hemolyse & cause the baby to be born with serious anemia.

Nucleated RBCs (Erythroblasts) appear in

the peripheral blood of

fetus. MCQ

Erythroblastosis Fetalis • Rh+ve RBCs in fetus are attacked by IgG antibodies by Rh – ve

hereditary spherocytosis

Cause: Hereditary spherocytosis is a genetic disorder caused by a variety

of molecular defects in the genes

that code for spectrin, ankyrin proteins. MCQ

RBCs are very small and spherical rather than being biconcave discs.

These cells cannot withstand

compression forces because they do

not have the normal loose, baglike

cell membrane structure of the biconcave discs.

On passing through the splenic pulp and some other tight vascular beds,

they are easily ruptured by even slight compression (increase fragility of RBCs). MCQ

hereditary spherocytosis • Cause: Hereditary spherocytosis is a genetic disorder caused by a variety of molecular

Polycythemia

It is a disease state in which the

proportion of blood volume that is

occupied by red blood cells increases.

Blood volume proportions can be measured as hematocrit level.

It can be due to an increase in the number of red blood cells("absolute polycythemia") or to a decrease in the volume of plasma ("relative polycythemia").

The emergency treatment of

polycythemia (e.g., in hyperviscosity or thrombosis) is removal of blood from the circulation.

Polycythemia • It is a disease state in which the proportion of blood volume that is

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 many

cells 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 in

the production of erythropoietin, hence an increased

production of RBCs. there may be 6-7 million/mm3 RBCs.

cause is treated.

Secondary polycythemia resolves when the underlying

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)

Effects of polycythemia on body

Headaches

Vertigo

abnormally enlarged spleen and/or liver.

increased viscosity of the blood

blood flow through the peripheral

blood vessels is often very sluggish.

Cardiac output does not change significantly.

Increase risk of thrombosis

Increase risk of cyanosis (>5 grams/dL deoxy Hb)

B.P. may rise in 1/3 of the patients

CYANOSIS IN POLYCYTHEMIA

CYANOSIS IN POLYCYTHEMIA