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51 Cards in this Set
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- 3rd side (hint)
I’m AML !! > Auer rod > myeloperoxidase!! Specific myleoid leukemia |
Back (Definition) |
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Reasons MC anemia |
>Iron deficient >Anemia of Chronic disease >Sideriblastic >Thalassemia ( 2condotion - mild / severe !) |
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Reason MC A |
Iron reduced Reduced heame synthesis Reduced globin synthesis |
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Iron deficiency |
> deficient diet... nalnutisguon Vegan ! Increased requirement.. pregnancy > blood loss.. less RBC,iron bloss > iron sequestration .. hypersplrnism.. ( soderoblastic anemia, cytocytosis, spherocytosis..) > |
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Iron deficiency- Feritin low Iron low !! TIBC UP!! - menorrhea - small bleeding - colon cancer ! Intuition bad !! Pregnancy !!
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Iron store depleted Iron serum low !! |
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Low iron serum Ferritin UP TIBC Low !! |
Chronic inflammation ! > autoimmune disease - SLE liver disease cancer Don’t release enough iron cause bacteria would use it !! |
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Reduced hem synthesis |
Lead posing Acquired / congenital sideroblastic anemia |
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Sideroblastic anemia Acquired / hero terry |
Shape of RBC like blasts ! Smear.. basophils stippling
Irreversible - myliduspataic subsiding Reversible - drugs , lead Alkohol |
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Reduced globin prediction Smear !! |
Thalassemia.. Aloha / beta 2) mild vs. severe ( transfusion ) Others : death ( 4 aploha - hydros fwtalsi ) Asymtopmtic ( 1 alpha / 0 beta deleted ) > Hypochrom > mucrocytitoc / teardrops ! |
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Transfusion in thalassemia |
Leads to hemosiserosis - treat with Deferixamine!! Hemoglobin electrophoresis - HgA1 ( normal adult ) 2a/2b HGF ( fetal ) 2a/2y |
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Iron - 1mg /2mg iron a day Absorption in duodenum!upoer part of Jejunum! Stored in liber., spleen, bone marrow Usuals in Muscle, bone marrow ! Iron absorption ! Hepcidin ! |
Therapy : ferrous - gluconate Fe - fumarate , sulphonate 3-6 month continue therapy ! |
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Iron absoprtion enhanced by |
Vit C Meat , fish, orange juice Inhibited by : cereals, tee, milk Side effects oral iron : heartburn, braids, abdominal cramps ! Diarrhea ! |
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Parenteral iron if |
Intolerance Gastrointestinal disorder ( chron, absipruon Problem ) Losses iron at rapid rate ( bleeding )
Side effects : pain flushing, lymph node enlarged, discoloration metallic taste Hypothesis, headache malade ! Urticaria nausea anaphylactic shock !! |
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Management of iron deficiency |
Intramuscular Parenteral Öl |
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Front (Term) |
Treat |
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Front (Term) |
Reduced intake . Loss high - bleeding Higher requirements . Pregnant |
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Physical signs |
Pallor, Jaimdice, ( hemolysis ) Lymphadenopathy Hepatosplebonefaly Bone pain Petechia Rectal / occult bleeding |
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Physical anemia |
Pallor - Skin, lips, nail bed /conjunctiva ! Nails - fragil ,flattened ,brittle spoon like, koilonychia Tongue / mouth -glissitis, angular cheliosis, stomatitis Dysphasia ( Peter- Kelly- OR Plummer Vinson Syndrom)= cancer in Situ!!! Stomach - atriphic gastritis ( malabsorption ! ) lessgastric secretions ! |
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Test MC anemia ! |
CBC ( number of cell ) Rwticulocute count ( production. Up / down ) Peripheral blood smear ! ( shape / which cells dominant ) |
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Bleeding test Hemolysis |
Hemolysis : LDL UP!! Haptiglibin down ! ,indirect bilirubin UP ! Cancer ( myleoplastic synd): all negative ( LDL, haptoglib, bilirubin) BUT blood smear positive !! Hemorrhage/ bleeding : LDL not elevated , Haptoglob bot down, bilirubin not up ! |
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Differential Blood loss Decreased production Increased destruction |
Iron deficient Aia Thalassemia Sideroblastic anemia A soma of chronic disease ! |
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Differentauma |
Difderent |
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Non immune Acquired / hereditary |
Hereditary - Membran defect : Cyto/ spherocytosis Enzym defect : G6 P D Hemoglobinopathoea > sickle cell > thalassemia Hb electrophoresis for diagnosis !! In children !! |
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Cold therapy |
Warm up ! Than corticosteroids ! Plasmaporesis!! Tongue riding IG! M |
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Warm type association |
Idiopathic : (in about 1/3 of cases)• 2. Secondary: • - lymphoid neoplasms: lymphoma, CLL, myeloma • - solid tumours: lung, colon, kidney, ovary, thymoma • - connective tissue disease: SLE, rheumatoid arthritis • - drugs: methyldopa,mefenamic acid, penicillin, quinine • miscellaneous: ulcerative colitis, HIV . |
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Acquired hemolysis |
1-Immune -warm antibody -cold antibody 2-Non immune -Microangiopathic hemolysis (DIC, TTP, Preeclampsia, eclampsia, HELLP , Drugs (mitomycin, cyclosporine) , Valvular hemolysis) -Infectious has - Paroxysmal nocturnal haemoglobinuria |
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Non immune hemolysis |
Infection - malaria Acquired defect- heart Microangiopathies - DIC TTP HUS... drugs , |
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Hemolysis |
Immune / non immune Immune : ABO system incompatible Infection / toxins Paroxysmal nocturnal hemolysis
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Acquired hemolytic |
> TTP > HUS ( hemolytic uremic Syndrom ) DIC Infection - malaria / barbiosis / lead poisoning |
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Autoimmune hemolytic syndrome |
Ig M/ G - autoimmune mediated Bilirubin up Haptoglibjn down - all 3 hemolysis ! LDH up
Cold type :Conpliment!! against RBC antigen sureface !! Warm - anitjbodies in patient blood bind to IGlobuline ig G !!on RBC !! Leading to macrophages activation in liver/ spleen (COMLiment activation ) -hemolysis !! Intravascular cellular !! Symphony in’s - anemia Splebimgeagly !! Ikterus Fever, spherocytosis !! ( also in hereditary spherocytosis ) Do combs test !! ( agglutinoations test ) blood IG against RBC !! |
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Symptoms aulimmune hemolytic 80% Warm type Strong conpliment !! Optimal temperature for AB functioning ! - extravascular hemolysis ! |
Anemia Splenimegaly Ikterus ( high UCB ) Fever , spherocytosis! ( peripheral blood smear )
Tjerr tree spy Highly dosed corticosteroid therapy !! 1mg / body W for 3 weeks !! Azathioprin!! Cyclosporine A for half a year !!max!! Retuximoab! After !!! Last resort ! Splenodectomy !! |
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Cold type - worse if anemia worsens in cold temperaturea ! Weak Conplimebt answer Cause to cold ! - intravadcualr hemolysis ! |
Ig M, against RBC antigen ! capacity to intravascular lysis. • Can be chronic when the antibody is monoclonal • They account cases. for the other 20% • Cold AIHA may be • 1. Idiopathic in associationwith lymphomas • 2. Secondary in certain infections like Mycoplasma pneumoniae |
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Therapy warm |
Warm ! Steroids Azatjioprim ! Cyclosporine Rituximab ! After 3 month - splenectomy ! |
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Warm type Associations |
Ret!! Count High! COOMBs Positiv ! • Variable anemianormochromic, spherocytes & micro- spherocytes with polychromasia |
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Cold type AIH |
Affect elderly may had low grade B cell lymphoma itravascular haemolysis with cold painful &blue fingers toes ears & nose. • red cell agglutination & may be high MCV. The patient must keep extremities warm some respond to corticosteroid. |
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Cold type |
• Normochromic, anisocytosis with autoagglutination,polychromasia • Direct Coomb’s tes is classically positive !! Same symptoms as warm type ! Pallor . Jaundice Vasocclusive !! Crisis ! - acrocyanosis in capillaries Splenomegaly |
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Sickle cell disease |
Anaemia • Jaundice • Splenomegaly Clinical features • Painful swelling hands &feet • Chronic lower leg ulcers probably arise fromischaemia & super infection in the distal circulation.
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Acquired haemoglobinopathies |
A.Methaemoglobin Sulfhaemoglobin C.Carboxyhaemoglobin HbH in erythroleukaemia |
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Acquired haemoglobinopathies |
A.Methaemoglobin Sulfhaemoglobin C.Carboxyhaemoglobin HbH in erythroleukaemia |
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I.Structural haemoglobinopathies—haemoglobins with altered amino acid sequences, eg. HbS II.Thalassaemias—defective |
biosynthesis of globin chains III.Thalassaemic haemoglobin variants—structurally abnormal Hb associated with co‐inherited thalassemic phenotype HbE,Hb Constant Spring,Hb LeporeI.Hereditary persistence of fetal haemoglobin |
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TTP (Thrombotic thrombocytopenia Prupira ) |
Sever thrombocytopenia ! Less 30 000 severe Under 10 000 therapy !! Treatment : 90‘% did ! Without restatement ! (20 with ) Palsmaphresis ! Daily ! With FFP !until tjrombocytoa mir Ethan 150 000 /L 1-3mg corticosteroids ! Azathioprin! Cyclosporine A, cyclophosphamide ! Thrombocyte aggregation inhib ! ASA! Dipyridamol! Ifthrombos over 100 G/ L Retuximqb ! NeVer give Thormbocyten !!! Eculizumab!!! Inhibits compliment system !! Splenectomy is nothing works !
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TTP hereditary / squired |
Enzym defect ! VWF cleaving - Protease NOt cleases !VWF ( ADAmTs-13) ! Not degradation of VWF - hyaline clot formation in vessel ! Thrombus !! > endothelial dampfe ! Clotting ! > |
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Clinic TTP |
LDH up ! Normal coagulation (pt) PPT CCT elevates, creation up ! Hematuria! Proteinyroa ! |
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Clinic TTP |
LDH up ! Normal coagulation (pt) PPT CCT elevates, creation up ! Hematuria! Proteinyroa ! |
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TTP |
Extra corpuscular hemolysis ! Hypoperfusuon organ !! Brain / kidney |
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ITP |
Peripheral blood smear > decreased number of platelets > large umature platelet > bone marrow - large Megakarypcytea |
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ITP |
Peripheral blood smear > decreased number of platelets > large umature platelet > bone marrow - large Megakarypcytea |
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ITP |
Best - mucous blessing !month Wet pup yea! Petechia ! Arms / legs Platelets massively low ! Could be leukemia !! As well !
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IPT 30-50- if symptoms ! Treat !! Under 30 also asymptomatic ! |
IV Ig ! 50-60% good prep sonar 2-3 days - high dose 1g / day ! Corticosteroids! Prednisone 2-3 mg / kg/ day 50 % good response ! |
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If relapse ! Biologically ! New drugs ! Thrombopoietin receptor agonist !! Vaccination ! |
immune globulin for Rh-positive patients (75 μg/kg) -Relapsed ITP (platelet count <30 x109/l): Rituximab, a monoclonal antibody to CD20. New drugs: TPO receptor agonists (Romiplostin, Eltrombopag) -
Splenectomy: if other treatments are ineffective. Laparoscopic mode, 2-3 weeks before operation: Pneumococcal, meningococcal, H. inf. Vaccination with response rate of 66% |
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Front (Term) |
Back (Definition) |
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