Blood

Red cells & anemia

By Hisham Almasry 11

RBCs formation

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Erythrocyte sedimentation rate (ESR)

This test is a measurement of non-specific plasma protein changes in disease

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Haemoglobin
Each molecule of normal adult haemoglobin (HbA) consists of four polypeptide chains 22, .

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Haemoglobin

Human Hb consists of
Haem =iron Globin Protien
4 amino acid chains Hb A >>>>>>2 +2 Hb A2>>>>>>2 +2 Hb F >>>>>>>2 +2
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Haemoglobin

The major switch from fetal to adult haemoglobin occurs 3-6 months after birth.

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Normal Hb in adult blood

Hb A Hb A2 Hb F

structure

a22

a2d2

a22

Normal %

96-98 %

1.5-3.2 %

0.5-0.8 %

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RBCs catabolism

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Normal red cell destruction

The breakdown of red cells liberates

1- iron for recirculation via plasma transferrin to marrow erythroblasts 2- protoporphyrin which is broken down to bilirubin. 3- globins which are converted to amino acids.

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Normal red cell destruction

The bilirubin circulates to the liver where it is conjugated to glucuronides which are excreted into the gut via bile and converted to stercobilinogen and stercobilin(excreted in faeces).

Stercobilinogen and stercobilin are partly reabsorbed and excreted in urine as urobilinogen and urobilin.

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Normal red cell breakdown

haemoglobin haem iron protoporphyrin globin Amino acids

transferrin erythroblast

Unconjugated Bilirubin (free)

Liver conjugation

Conjugated Bilirubin

Urine

faeces

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What does the body need to make RBCs??

Bone marrow ( the factory ) Erythropoietin ( the stimulator ) Iron Vit. B12
Vitamins ( B1 , B6 , C , E ) Metals
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RBCs tests
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Red Blood Cell Count

Male 4.26.1 1012/L Female 4.25.4 1012/L

Haemoglubin
Male 13.018.0 g/dL Female 11.516.5 g/dL

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Haematocrit (packed cell volume or PCV)

Male 4054%; Female 3747%

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RBCs tests contd

Mean cell volume(MCV)

femtoliters (fl; 10-15 liters). MCV = PCV/RBCs = 45 / 5 >>>>>>7899 fL

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Mean cell haemoglobin(MCH)

units are picograms (pg) per cell MCH = Hb/RBC = 15 / 5 >>>>>>2731 pg

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Mean cell haemoglobin Concentration (MCHC)

MCHC = Hb/PCV = 15 / 45 >>>>>>>3236 g/dL

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RBCs disorders

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Anemia

Its classified according to the RBCs volume (M.C.V) & haemoglobin content (M.C.Hb) >>>>>>>>>three categories

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Main signs and symptoms

Sings and symptoms: Pallor Dysnea Disiness Palpitation Glossitis

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Anemia
80-95 fl M.C.Hb >27 pg

Normocytic normochromic
.C.V <80 fl M.C.Hb <27 pg

icrocytic hypochromic M.C.V

Macrocytic normochromic M.C.V >95

Iron deficiency anemia thalaessemia

Blood loss B12 deficiency Haemolytic anemia (prenicious anemia) Aplastic anemia G6PD anemia Folate deficiency Sickle cell anemia (megaloblastic anemia)

fl M.C.Hb >27 pg

Anemia of chronic disease

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Iron deficiency anemia

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Microcytic hypochromic

Fe is very important for Hb synthesis Any change in iron ratio in blood will cause that disease Cause involve :
1. 2. 3.

Iron deficiency anemia

decrease iron intake increase iron loss in bleeding ( more in females ) decrease in iron absorption cancer caecum

Body storage 3 g Daily intake 10 mg/d

(vit. C increase , tannic acid decrease )

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Main symptoms + koilynychia Atrophic glossitis >>>>> (plumer vinson syndrome )

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Investigations :

MCV MCHb Ferritin

Iron deficiency anemia

Iron binding capacity

TTT: Ferrous sulphate capsules

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Microcytic hypochromic

Absence of one or both of the or chains -thalassaemia -thalassaemia

No chain Patient with 4 B chains called Hb barts Usually dies before birth

Thalassaemia

heterozygous
Asymptomatic Hypochromic microcytic anaemia homozygous

Hb f Marked anaemia Extramedullary haemopiosis Hepatospleenomegally Skeletal changes

2727 TTT regular blood transfusion or bone marrow transplantation

Expansion of the bone marrow: thalassaemia

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Thalassaemia

Dental implications : Bossing of the skull Bones are brittle Problems with GA Recurrent infections

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Normocytic normochromic

Haemolytic anemia

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Normocytic normochromic

Haemolytic Any destructionanemia in the RBCs

Immune causes:

Maybe autoimmune disease Maybe incompatible bl. Transfer Lymphoma CLL leukemia

Non immune causes

Hb abnormalities In enzyme that protect cell wall from damage (G6PD-deficiency) Drugs ( sulphasalazine)

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Normocytic normochromic

Aplastic anemia

Complete or partial loss of precursor cells of RBCs, WBCs & platelets Causes:

Congenital Viral infection( TB, hepatitis ) Drugs ( chloramphenicol) Radiology Renal failure Heavy metal poisoning

Diagnosis : Pancytopenia Bone marrow smear>>>>>> hypocellular (fibrofatty tissues) TTT : bone marrow transplantation

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Normocytic normochromic

Abnormal arrangment of the amino acids in the chain Causes sickling of the RBCs 2 types.

Sickle cell anemia

Heterogenous
HBAs Abnormal Hb <50% Clinical problems only in sever hypoxia

Homogenous

HBSS Abnormal Hb > 50% Sever clinical symptoms

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Increase rigidity and aggregation in micro-circulation Sickling crisis assossiated with bone pain Preciptated by: Infection Dehydration Low temp. Complications: Renal damage infarctions Aseptic bone necrosis specially in the premaxilla.

Sickle cell anemia

TTT..no TTT , just avoid dehydration and hypothermia

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Sickle cell anemia

Dental implications: Problems with the GA Treat infections with antibiotics Aseptic bone necrosis
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Macrocytic normochromic

B12 deficiency anemia

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Macrocytic normochromic

B12 deficiency The intrinsic factor secreted from the parietal cells is anemia responsible of the absorption of vit.B12

Vit.B12 is important for the maturation of the RBCs, If absent the cells will abnormal cell growth and maturation. If there is AB against parietal cells it will be called pernicious anemia

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Causes:

Vegan diet

B12 deficiency anemia

Partial gastrectomy Antibodies to IF or the parietal cells

Investigations:

MCV >100 serum B12 Parietal cells AB Schilling test

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B12 deficiency TTT anemia

IF Cyanocoblamine (vit. B12)

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Macrocytic normochromic

Folic acid deficiency anemia (megaloblastic anemia)

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crocytic normochromic

Folic acid deficiency anemia (megaloblastic anemia) Has the same function as vit.B12
Deficiency leads to the production of large cells (macrocytes) some of which may remain primitive with nuclei (megaloblasts) Causes Dietary deficiency Malabsorption TTT>>>>>>>>>>>>>>oral folate therapy 5-10 mg folic acid daily
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Leukemia

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abnormal infilteration of the bone marrow by immature cells

Myeloblast

Leukemi a
Acute Chronic

Lymphoblast

AML
Myelocyte Lymphocyte

ALL

CML
Reticulocyte

CLL
Mature T & B

RBCs

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Leukemia

The accumulation of the immature cells in the bone marrow >>>>>>>> B.M failure
>>>>>anaemia >>>>>leucopenia >>>>>thrombocytopenia >>>>>hepatomegaly & spleenomegaly C/P Tiredness , malaise , pyrexia , signs of anaemia (night sweats)

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Dental implications
Bleeding

Leukemia

Gingival hyperplasia ( fragile & bleeding) Orodental infections ( should be treated aggressively due to lack of neutrophils
Fungal ( candidosis) Bacterial (ANUG) viral (HSV , CMV , HZ ) EBV >>>> hairy leukoplakia
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Leukemia

TTT Alkylating agents Spleenectomy leucophoresis

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Lymphoma
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Lymphoma

Abnormal proliferation of diff. parts of lymphatic system

Fever Wt loss Drenching night sweat

Non hodgkins lymphoma

Middle or old age No RS cells Etiology maybe viral HIV , EBV

Hodgkins lymphoma
Young age Reed sternberg cells Painless lymphadenopathy (neck and axillae ) Nodes are rubbery and firm
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Lymphoma

TTT>>>>> radiotherapy or chemotherapy Radiotherapy has some side effects

Damage to salivary glands ( xerostomia) Damage to bone ( osteoradionecrosis) Damage to lungs ( pneumonitis) Mucous membrane ( mucositis & recurrent infection)
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Lymphoma

clinical staging, as follows: - I: Involvement of a single group of lymph nodes - II: Involvement of two or more groups of lymph nodes on the same side of the diaphragm - III: Involvement of lymph nodes on both sides of the diaphragm - IV: Involvement of extralymphatic organs (liver, bones, etc.)
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Lymphoma

Dental implications :
I. II. III. IV. V.

Plan ttt before radiation Antibacterial mouthwashes Treat the fungal and bacterial infections Treat the dry mouth with artificial saliva Always suspect recurrent tumors
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