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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
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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.
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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
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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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Click to edit Master text stylesSecond level
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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Click to edit Master text stylesSecond level
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)
ormocytic normochromic
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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
ormocytic normochromic
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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
ormocytic normochromic
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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
acrocytic normochromic
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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)
acrocytic normochromic
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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