blood anemia&leukemia1

8/3/2019 blood anemia&leukemia1

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Red cells & anemia

Blood

ByHisham Almasry

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RBCs formation

Click to edit Master text stylesSecond level Third level

Fourth level Fifth level

RBCs life cycle is 120 days

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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 normaladult haemoglobin (Hb-

A) consists of fourpolypeptide chains

22,

.

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Haemoglobin

Human Hb consists of

Haem=iron

GlobinProtien

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

destructionThe breakdown of red cells liberates

1- iron for recirculation via plasma transferrin to marrowerythroblasts

2- protoporphyrin which is broken down to bilirubin.

3- globins which are converted to amino acids.

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Normal red cell

destructionThe bilirubin circulates to the liver where it is conjugated to glucuronideswhich are excreted into the gut via bile and converted to stercobilinogenand stercobilin(excreted in faeces).

Stercobilinogen and stercobilin are partly reabsorbed and excreted inurine as urobilinogen and urobilin.

1111

N l d ll b kd


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Normal red cell breakdown

haemoglobin

haem

protoporphyriniron

Unconjugated Bilirubin(free)transferrin

erythroblastConjugated Bilirubin

Urine

Liver conjugation

faeces

globin

Amino acids

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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

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

Haematocrit (packed cell volume or PCV)

Male 4054%;

Female 3747%

5

15

45

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Mean cell volume(MCV)femtoliters (fl; 10-15 liters).

MCV = PCV/RBCs

= 45 / 5

>>>>>>7899 fL

Mean cell haemoglobin(MCH)units are picograms (pg) per cellMCH = Hb/RBC

= 15 / 5>>>>>>2731 pg

Mean cell haemoglobin Concentration (MCHC)

MCHC = Hb/PCV= 15 / 45

>>>>>>>3236 g/dL

90

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RBCs tests contd

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Click to edit Master text stylesSecond level

Third level

Fourth level Fifth level

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Click to edit Master title style

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RBCsdisorders

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Click to edit Master title style

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AnemiaIts 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

PalpitationGlossitis

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Anemia

icrocytic hypochromic

.C.V 95

fl

M.C.Hb >27pg

Iron deficiency anemiathalaessemia

Blood lossHaemolytic anemiaAplastic anemiaG6PD anemiaSickle cell anemia

B12 deficiency(prenicious anemia)

Folate deficiency

(megaloblastic anemia)

Anemia of chronic disease

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Iron deficiency

anemia

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Iron deficiencyanemiaFe is very important for Hb synthesis

Any change in iron ratio in blood will cause that disease

Cause involve :

1. decrease iron intake2. increase iron loss in bleeding ( more in females )

3. decrease in iron absorption

(vit. C increase , tannic acid decrease )

4. cancer caecumMain symptoms +

koilynychia

Atrophic glossitis >>>>> (plumer vinson syndrome )

icrocytic hypochromic Body storage 3 gDaily intake 10 mg/d

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Third level Fourth level

Fifth level

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Iron deficiencyanemiaInvestigations :

MCV MCHb

Ferritin Iron binding capacity

TTT:

Ferrous sulphate capsules

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Thalassaemia-thalassaemia

No chain

Patient with 4 B chains called Hb barts

Usually dies before birth

icrocytic hypochromic

-thalassaemia

homozygous

heterozygous

Hb f

Marked anaemia

Extramedullary haemopiosis

Hepatospleenomegally

Skeletal changes

Asymptomatic

Hypochromic microcytic

anaemia

TTT regular blood transfusion or bone marrow transplantation

Absence of one or both of the or chains

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Third level Fourth level

Fifth level

Expansion of the bone marrow: thalassaemia

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ThalassaemiaDental implications :

Bossing of the skull

Bones are brittle

Problems with GA

Recurrent infections

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Haemolyticanemia

ormocytic normochromic

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HaemolyticanemiaAny destruction 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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Aplastic anemiaComplete 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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Sickle cellanemiaAbnormal arrangment of the amino acids inthe chain

Causes sickling of the RBCs

2 types.

HeterogenousHBAsAbnormal Hb 50%Sever clinical symptoms


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Sickle cellanemiaIncrease 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.

TTT..no TTT , just avoid dehydration and hypothermia

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Sickle cellanemia

Dental implications:

Problems with the GA

Treat infections with antibioticsAseptic bone necrosis

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B12 deficiencyanemia

acrocytic normochromic

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B12 deficiencyanemiaThe intrinsic factor secreted from the parietal cells isresponsible of the absorption of vit.B12

Vit.B12 is important for the maturation of the RBCs,If absent the cells will abnormal cell growth andmaturation.

If there is AB against parietal cells it will be calledpernicious anemia


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B12 deficiencyanemiaCauses:

Vegan diet

Partial gastrectomy

Antibodies to IF or the parietal cells

Investigations:

MCV >100

serum B12 Parietal cells AB

Schilling test

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B12 deficiencyanemiaTTT

IF

Cyanocoblamine (vit. B12)

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Folic acid deficiency anemia

(megaloblastic anemia)


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Folic acid deficiency

anemia(megaloblastic anemia)Has the same function as vit.B12Deficiency leads to the production of large cells(macrocytes) some of which may remain primitive withnuclei (megaloblasts)

Causes

Dietary deficiency

MalabsorptionTTT>>>>>>>>>>>>>>oral folate therapy

5-10 mg folic acid daily

crocytic normochromic

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Leukemia

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Leukemia

abnormal infilteration of the bone marrow by immature cells

Myeloblast

Myelocyte

Lymphoblast

Lymphocyte

Reticulocyte

RBCs

Mature T & B

Acute

Chronic

AML ALL

CMLCL

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LeukemiaThe accumulation of the immature cells in the bonemarrow >>>>>>>> B.M failure

>>>>>anaemia

>>>>>leucopenia

>>>>>thrombocytopenia

>>>>>hepatomegaly & spleenomegaly

C/P

Tiredness , malaise , pyrexia , signs of anaemia (night sweats)

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Dental implications

Gingival hyperplasia ( fragile & bleeding)

Bleeding

Orodental infections ( should be treatedaggressively due to lack of neutrophils

Fungal ( candidosis)

Bacterial (ANUG)

viral (HSV , CMV , HZ )

EBV >>>> hairy leukoplakia

Leukemia

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LeukemiaTTT

Alkylating agents

Spleenectomy

leucophoresis

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Lymphoma

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Lymphoma

Non hodgkinslymphoma

Middle or old age

No RS cells

Etiology maybe viral

HIV , EBV

Hodgkinslymphoma

Young age

Reed sternberg cells

Painless lymphadenopathy (neckand axillae )

Nodes are rubbery and firm

Abnormal proliferation of diff. parts of lymphatic systemFever

Wt loss

Drenching night sweat

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LymphomaTTT>>>>> 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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Lymphomaclinical staging, as follows:

- I: Involvement of a single group of lymph nodes

- II: Involvement of two or more groups of lymph nodes onthe same

side of the diaphragm

- III: Involvement of lymph nodes on both sides of thediaphragm

- IV: Involvement of extralymphatic organs (liver, bones,etc.)

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LymphomaDental implications :

I. Plan ttt before radiation

II. Antibacterial mouthwashes

III. Treat the fungal and bacterial infections

IV. Treat the dry mouth with artificial saliva

V. Always suspect recurrent tumors

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