JSC “Astana Medical University” Department of Internal Disease IWS Theme:

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1. JSC “Astana Medical University” Department of Internal Disease IWS Theme:
2. Слайд 2
3. Hemolytic AnemiaDefinition:Those anemias which result from an increase in RBC destructionClassification:Congenital / HereditaryAcquired
4. Ref : Harrison’s
5. Слайд 5
6. Слайд 6
7. Hemoglobinuria
8. Features of HEMOLYSISBilirubinLDHReticulocytes, n-RBCHaptoglobulins+ve Urinary hemosiderin, UrobilinogenBlood
9. Слайд 9
10. Red Cell Membrane Defects1.Hereditary SpherocytosisUsually inherited as
11. C/F:AsymptomaticFluctuating hemolysisSplenomegalyPigmented gall stones- 50% Clinical course
12. 2.Hereditary ElliptocytosisEquatorial Africa, SE AsiaAD / ARFunctional
13. 1. Glucose-6-Phosphate Dehydrogenase ( G6PD ) DeficiencyPivotal
14. Clinical Features:Acute drug induced hemolysis:Aspirin, primaquine, quinine,
15. Autoimmune Hemolytic AnemiaResult from RBC destruction due
16. 1.Warm AI Hemolysis:Can occurs at all age
17. IMMUNOHEMOLYTIC ANEMIAMACROCYTESPHEROCYTE
18. Direct antiglobulin test demonstrating the presence of
19. Inv:e/o hemolysis, MCV P Smear: Microspherocytosis, n-RBCConfirmation:
20. 2. Cold AI HemolysisUsually Ig MAcute or
21. Non-Immune Acquired Hemolytic Anemia1. Mechanical TraumaA). Mechanical
22. ReferencesClinical Analysis and Synthesis of Symptoms and
23. Скачать презентанцию

Hemolytic AnemiaDefinition:Those anemias which result from an increase in RBC destructionClassification:Congenital / HereditaryAcquired

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JSC “Astana Medical University” Department of Internal Disease IWS Theme:

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Слайд 1
JSC “Astana Medical University”
Department of Internal Disease

IWS
Theme: Hemolytic anemia

Checked by: Baidurin S. A.
Done by: Zarlykanov S.

Astana 2018

Слайд 3Hemolytic Anemia

Definition:
Those anemias which result from an increase in RBC

destruction

Classification:
Congenital / Hereditary
Acquired

Слайд 4Ref : Harrison’s

Слайд 7Hemoglobinuria

Слайд 8Features of HEMOLYSIS
Bilirubin
LDH
Reticulocytes, n-RBC
Haptoglobulins
+ve Urinary hemosiderin, Urobilinogen

Blood Film

Spherocytes

No spherocytes Fragmentation

DCT +ve

DCT –ve

AI Hemolysis H. Sherocytosis Malaria,
Clostidium
Hereditery enzymopathies Microangiopathic, Traumatic

Features of HEMOLYSISBilirubinLDHReticulocytes, n-RBCHaptoglobulins+ve Urinary hemosiderin, UrobilinogenBlood FilmSpherocytes No spherocytes

Слайд 10Red Cell Membrane Defects
1.Hereditary Spherocytosis
Usually inherited as AD disorder
Defect: Deficiency

of Beta Spectrin or Ankyrin  Loss of membrane in

Spleen & RES becomes more spherical Destruction in Spleen

Red Cell Membrane Defects1.Hereditary SpherocytosisUsually inherited as AD disorderDefect: Deficiency of Beta Spectrin or Ankyrin  Loss

Слайд 11C/F:
Asymptomatic
Fluctuating hemolysis
Splenomegaly
Pigmented gall stones- 50%
Clinical course may be complicated

with Crisis:
Hemolytic Crisis: associated with infection
Aplastic crisis: associated with Parvovirus

infection

Inv:
Test will confirm Hemolysis
P Smear: Spherocytes
Osmotic Fragility: Increased

Osmotic Fragility

C/F:AsymptomaticFluctuating hemolysisSplenomegalyPigmented gall stones- 50% Clinical course may be complicated with Crisis:Hemolytic Crisis: associated with infectionAplastic crisis:

Слайд 122.Hereditary Elliptocytosis
Equatorial Africa, SE Asia
AD / AR
Functional abnormality in one

or more anchor proteins in RBC membrane- Alpha spectrin ,

Protein 4.1
Usually asymptomatic
Mx: Similar to H. spherocytosis
Variant:
3.SE-Asian ovalocytosis:
Common in Malaysia , Indonesia…
Asymptomatic-usually
Cells oval , rigid ,resist invasion by malarial parasites

Elliptocytosis

Слайд 131. Glucose-6-Phosphate Dehydrogenase ( G6PD ) Deficiency
Pivotal enzyme in HMP

Shunt & produces NADPH to protect RBC against oxidative stress
Most

common enzymopathy -10% world’s population
Protection against Malaria
X-linked

1. Glucose-6-Phosphate Dehydrogenase ( G6PD ) DeficiencyPivotal enzyme in HMP Shunt & produces NADPH to protect RBC

Слайд 14Clinical Features:
Acute drug induced hemolysis:
Aspirin, primaquine, quinine, chloroquine, dapsone….
Chronic compensated

hemolysis
Infection/acute illness
Neonatal jaundice
Favism

Inv:
e/o non-spherocytic intravascular hemolyis
P. Smear: Bite cells, blister

cells, irregular small cells, Heinz bodies, polychromasia
G-6-PD level

Treatment:
Stop the precipitating drug or treat the infection
Acute transfusions if required

Clinical Features:Acute drug induced hemolysis:Aspirin, primaquine, quinine, chloroquine, dapsone….Chronic compensated hemolysisInfection/acute illnessNeonatal jaundiceFavismInv:e/o non-spherocytic intravascular hemolyisP. Smear:

Слайд 15Autoimmune Hemolytic Anemia
Result from RBC destruction due to RBC autoantibodies:

Ig G, M, E, A
Most commonly-idiopathic
Classification
Warm AI hemolysis:Ab binds at

37degree Celsius
Cold AI Hemolysis: Ab binds at 4 degree Celsius

Autoimmune Hemolytic AnemiaResult from RBC destruction due to RBC autoantibodies: Ig G, M, E, AMost commonly-idiopathicClassificationWarm AI

Слайд 161.Warm AI Hemolysis:
Can occurs at all age groups
F > M
Causes:
50%

Idiopathic
Rest - secondary causes:
1.Lymphoid neoplasm: CLL, Lymphoma, Myeloma
2.Solid Tumors: Lung,

Colon, Kidney, Ovary, Thymoma
3.CTD: SLE,RA
4.Drugs: Alpha methyl DOPA, Penicillin , Quinine, Chloroquine
5.Misc: UC, HIV

1.Warm AI Hemolysis:Can occurs at all age groupsF > MCauses:50% IdiopathicRest - secondary causes:1.Lymphoid neoplasm: CLL, Lymphoma,

Слайд 17 IMMUNOHEMOLYTIC ANEMIA
MACROCYTE
SPHEROCYTE

Слайд 18Direct antiglobulin test demonstrating the presence of autoantibodies (shown here)

or complement on the surface of the red blood cell.

complement

Слайд 19Inv:
e/o hemolysis, MCV
P Smear: Microspherocytosis, n-RBC
Confirmation: Coomb’s Test /

Antiglobulin test

Treatment
Correct the underlying cause
Prednisolone 1mg/kg po until Hb reaches

10mg/dl then taper slowly and stop
Transfusion: for life threatening problems
If no response to steroids  Spleenectomy or,
Immunosuppressive: Azathioprine, Cyclophosphamide

Inv:e/o hemolysis, MCV P Smear: Microspherocytosis, n-RBCConfirmation: Coomb’s Test / Antiglobulin testTreatmentCorrect the underlying causePrednisolone 1mg/kg po

Слайд 202. Cold AI Hemolysis
Usually Ig M
Acute or Chronic form
Chronic:
C/F:
Elderly patients

Cold , painful & often blue fingers, toes, ears, or

nose ( Acrocyanosis)
Inv:
e/o hemolysis
P Smear: Microspherocytosis
Ig M with specificity to I or I Ag

2. Cold AI HemolysisUsually Ig MAcute or Chronic formChronic:C/F:Elderly patients Cold , painful & often blue fingers,

Слайд 21Non-Immune Acquired Hemolytic Anemia
1. Mechanical Trauma
A). Mechanical heart valves, Arterial

grafts: cause shear stress damage
B).March hemoglobinuria: Red cell damage in

capillaries of feet
C). Thermal injury: burns
D). Microangiopathic hemolytic anemia (MAHA): by passage of RBC through fibrin strands deposited in small vessels  disruption of RBC eg: DIC,PIH, Malignant HTN,TTP,HUS

Non-Immune Acquired Hemolytic Anemia1. Mechanical TraumaA). Mechanical heart valves, Arterial grafts: cause shear stress damageB).March hemoglobinuria: Red

Слайд 22References
Clinical Analysis and Synthesis of Symptoms and Signs on Pathophysiologic

Basis, JULIUS BAUER

Clinical Medicine, Kumar & Clark

Cecil textbook of medicine

Harrison’s

principles of Internal Medicine

ReferencesClinical Analysis and Synthesis of Symptoms and Signs on Pathophysiologic Basis, JULIUS BAUERClinical Medicine, Kumar & ClarkCecil

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JSC “Astana Medical University” Department of Internal Disease IWS Theme:

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Слайд 1 JSC “Astana Medical University”Department of Internal Disease IWSTheme: Hemolytic anemia

Слайд 2

Слайд 3Hemolytic AnemiaDefinition:Those anemias which result from an increase in RBC

destructionClassification:Congenital / HereditaryAcquired

Слайд 4Ref : Harrison’s

Слайд 5

Слайд 6

Слайд 7Hemoglobinuria

Слайд 8Features of HEMOLYSISBilirubinLDHReticulocytes, n-RBCHaptoglobulins+ve Urinary hemosiderin, UrobilinogenBlood FilmSpherocytes

No spherocytes FragmentationDCT +ve

Слайд 9

Слайд 10Red Cell Membrane Defects1.Hereditary SpherocytosisUsually inherited as AD disorderDefect: Deficiency

of Beta Spectrin or Ankyrin  Loss of membrane in

Слайд 11C/F:AsymptomaticFluctuating hemolysisSplenomegalyPigmented gall stones- 50% Clinical course may be complicated

with Crisis:Hemolytic Crisis: associated with infectionAplastic crisis: associated with Parvovirus

Слайд 122.Hereditary ElliptocytosisEquatorial Africa, SE AsiaAD / ARFunctional abnormality in one

or more anchor proteins in RBC membrane- Alpha spectrin ,

Слайд 131. Glucose-6-Phosphate Dehydrogenase ( G6PD ) DeficiencyPivotal enzyme in HMP

Shunt & produces NADPH to protect RBC against oxidative stressMost

Слайд 14Clinical Features:Acute drug induced hemolysis:Aspirin, primaquine, quinine, chloroquine, dapsone….Chronic compensated

hemolysisInfection/acute illnessNeonatal jaundiceFavismInv:e/o non-spherocytic intravascular hemolyisP. Smear: Bite cells, blister

Слайд 15Autoimmune Hemolytic AnemiaResult from RBC destruction due to RBC autoantibodies:

Ig G, M, E, AMost commonly-idiopathicClassificationWarm AI hemolysis:Ab binds at

Слайд 161.Warm AI Hemolysis:Can occurs at all age groupsF > MCauses:50%

IdiopathicRest - secondary causes:1.Lymphoid neoplasm: CLL, Lymphoma, Myeloma2.Solid Tumors: Lung,

Слайд 17 IMMUNOHEMOLYTIC ANEMIAMACROCYTESPHEROCYTE