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Hematology Module 2 > module 7 hemolytic anemia > Flashcards

module 7 hemolytic anemia Flashcards

1
Q

signs increased RBC production:

A

RPI >2, inceased IRF, leukocytosis, nucleated RBCs, polychromasia of RBCs, normoblastic erythroid hyperplasia.

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2
Q

signs increased RBC destruction

A

Anemia, schistocytes, spherocytes, positive DAT, decreased haptoglobin andhemopoexin, increased billirubin and urobillinogen, increased serum LD, increased CO.

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3
Q

Signs increased IV hemolysis

A

hemoglobinemia and uria, hemosiderinuria, methemoglobinemia

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4
Q

clinical findings HA

A

jaundice, gallstones, dark or red urine in IV hemolysis, anemia, thinning cortical bone, Extramedullary hematopoeisis, splenomegaly.

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5
Q

loss of vertical interactions

A

cause microvessicles and spherocytes (ankyrin, band 4 protein 4.2)

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6
Q

loss of horizontal interactions leads to

A

poikilocytes (spectrin, actin, protein 4.1, GPC)

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7
Q

acanthocyte

A

spiked membrane, excess in outer layer

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8
Q

stomatocyte

A

looks like kissing lips or coffee bean,

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9
Q

lipid composition defects characterized by

A

acanthocytes

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10
Q

Hereditary spherocytosis

A

deficient in membrane proteins, permeable monovalent cations. Often combined spectrin ankyrin deficiency. Membrane loss causes decreased SA to volume ratio and spherocyte. More permeable to Na, causing pumps to work harder expend more glucose. Can be well compensated. Can have aplastic crisis after viral infection.

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11
Q

HS LAB RESULTS

A

Reticulocyte count > 8%. MCHC increased. MCV decreased. increased billirubin, increased LD.

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12
Q

Osmotic fragility test

A

incubate in varying NaCl solutions. HS hemolyze at higher salt concentrations than normal. Little water can be absorbed before lysis. If < 2% spherocytes, incubate overnight at 37C before addition to NaCl. Increases SA loss and spherocyte formation.

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13
Q

Target cells and thalassemia in osmotic fragility test

A

target cells such as those in thalassemia shift to right because lysis occurs at lower NaCl concentration due to increased SA to volume ratio.

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14
Q

Autohemolysis test

A

incubate cells at 37C. Increased hemolyisis due to membrane chages. corrected by addition of glucose. Autohemolyisis increases in immunue hemoluytic anemia, but glucose does not correct.

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15
Q

HS and HE shape acquired

A

in the circulation, not created with misshape.

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16
Q

HE defect

A

horizontal interactions, such as: defective spetrin chains decrease dimer : tetramer ratio, band 4.1 defect, , abnormal GPC/ band 3.

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17
Q

HE clinical findings

A

hemolysis mild and well compensated. Membrane more rigid, may provide malaria defense.

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18
Q

HE lab findings

A

> 25 % elliptocytes. Osmotic fragility positive but not necessary as picture is obvious. Responds well to splenectomy.

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19
Q

HPP defect

A

disintegrate at 45-46C unlike normal at 50C. or >37C for 6 hours. Due to inheritance of both a mutant spectrin and a decreased expression spectrin gene. Disruption membrane, fragmentation, poikilocytosis.

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20
Q

HPP clinical and lab finding

A

exchange transfuion needed. bizarre shapes. Extreme microcytosis 25-55 fL MCV. Osmotic fragility abnormal after incubation and heat. Autohemolysis not corrected by glucose. SPlenectomy.

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21
Q

Overhydragted hereitary stomatocytosis

A

Gain of Na+ which exceeds K+ loss. Water enters cell, causes formation of stomatocyte.

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22
Q

dehydrated hereditary spherocytosis

A

Loss of K+ which exceeds Na gain. water leaves cell, becomes targeted.

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23
Q

HSS clinical and lab findings

A

abnormal cation permeability. mild to moderate anemia, 10-50% stomatocytes. osmotic fragility and autohemolysis increased, partially corrected by glucose.

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24
Q

acanthocytosis

A

increased sphingomyelin secondary to plasma changes. expansion of outer leaflet, decreased deformability. Not due to proteins. Abetalipoproteinemia, spur cell anemia,

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25
Q

glucose corrects for autohemolysis test in

A

HS not IHA.

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26
Q

SPUR CELL ANEMIA

A

type acanthocytosis associated with liver disease.

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27
Q

G6PD

A

first step in Hexose monophosphate shunt for GSH. Therefore responsible for preventing cellular oxidation.

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28
Q

Oxidation causes

A

iron oxidation and sulfahydryl groups of globin. Cannot bind oxygen, heinz bodies. Ion proetins and lipids also need to stay reduced.

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29
Q

Bite and Blister cells

A

G6PD deficiency. Splenic macrophages take bite out of cell. MCV goes down, MCHC goes up. Can cause spherocytes.

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30
Q

Detect G6PD deficiency

A

spectrometry flourescencePCR.

31
Q

Pyruvate Kinase

A

important in glycolytic pathwy. Deficeincy leads to Echinocytes, target cells, and HJ bodies.

32
Q

Hemolysis in pyruvate kinase often compensated by

A

2-3 BPG overproduction, decreases oxygen affinity.

33
Q

Micrangiopathy HA (MAHA)

A

thrombii in circulation. Fibrin deposits in vasculature damages RBC membrane

34
Q

TPP

A

microclots damage RBCs. Usually follow infection or pregnancy. Similar to HUS.

35
Q

DIC

A

often from bacterial blood infection, platelets consumed. Clots damage RBCs. Clotting time extended, abnormal bleeding, blood flow impeded to organs. Multiple organ faiilure. Abnormal coagulation tests differentiate it from TTP and HUS.

36
Q

babesia

A

normally mild anemia like malaria. transmitted by ticks. PCR and serological tests to dif from malaria.

37
Q

complement fixation

A

recruiting complement by antibodies.

38
Q

IGG

A

warm reactive

39
Q

IGM

A

cold reactive

40
Q

Contrast warm and cold acting hemolysis

A

Splenic macrophages have direct FCrIGG and can EV hemolyze. IGM can be IV through complement, or EV hrough c3b R on macrophages.

41
Q

AlloAb Hem Anemia examples

A

HDFN, blood transfusions.

42
Q

IGM complement activation

A

only one molecule of IGG required to activated classical pathway, therefore much more sensitive. 2 in close proximity required for IGG.

43
Q

IGM detection on RBC

A

antisera can detect IGM on RBC via agglutination in saline. Zeta potential and size of IGG prevents agglutination.

44
Q

Direct Anti human Globulin test (DAT or direct coombs)

A

Polyspecific AHG is added, agglutination means either the anti IGG or the anti complement antibodies have bridged zeta potential and caused agglutination. Follow with monospecific AHG. If only complement then likely IGM.

45
Q

IAT indirect anti human globulin or indirect coombs

A

Detects antibody in plasma. Less Ab required. Ab incubated with known antigenic makeup screening cells. Then add AHG positive if agglutination.

46
Q

pathophysiology WAIHA

A

most auto Ab against Rh antigens. common in CLL, neoplastic syndromes, autoimmune disorders. Most hemolysis EV.

47
Q

Clinical and Lab findings

A

Splenomegaly common. Positiv DAT, normocytic normochromic. increased LD, billirubin. Decreased haptoglobin. Increased osmotic fragility. Spherocytes, increased RDW compared to HS.

48
Q

Distinguish HS from WAIHA

A

DAT. Increased RDW.

49
Q

WAIHIA therpay

A

Alloantibodies make transfusion difficult. Focus is on preventing auto Ab formation: corticosteroids, splenectomy, IVIG \, plamapheresis.

50
Q

Cold Agglutination Syndrome

A

Mostly IGM against I antigens. Splenomegaly. Often episodic.

51
Q

Raynaud’s phenmomena

A

pain and cyanosis in extremeties due to cold agglutination of IGM.

52
Q

CAS Lab findings

A

RBC count decreased for hemoglobin, MCV is falsely elevated due to agglutination. Must warm all reagents and bood to 37C. When warm, normocytic normochromic, spherocytes, rolouex, nucleated RBCS. Dat poly and complement positive, IGG negative.

53
Q

Cold agglutinin test

A

Titer at which cells agglutinate. For benign cold agglutinins 1:50 or less. For CAS 1:1000.

54
Q

CAS therapy

A

corticosteroids, keep hands warm. Plasma exchange. Splenectomy not effective.

55
Q

Paroxsymal Cold hemoglobinuria

A

common in children. Generally appears weeks after certain infections, persists month or more. IGG antibody against p antigens. Biphasic, complement fixation. Hemoglobinuria, jaundice, splenomegaly.

56
Q

PCH clinical findings

A

weak or no DAT to complement. Can be positive for IAT if done at low temperature. HB levels drop following an attack and appear in blood and urine. Classic IV signs and neutropenic shift to left. No therapy, recover after infection.

57
Q

PCH specific test

A

incubate two tubes one at 37 one at 4C. Then incubate both at 37. Lysis in the 4C tube confirms PCH.

58
Q

Drug dependent and independent antibodies

A

describes whether the drug presence is required for the antibodies to react.

59
Q

Drug independent Ab mechanism

A

usually modifies antigens so no longer recognized as self. Drugs can also alter the membrane so that ab can bind non specifically. DAT positive, complement negative.

60
Q

Hemolytic transfusion reaction

A

Patients alloantibodies destroy donors RBCs. Immediate usually ABO and IGM can be IV. Delayed: previously sensitized but not detectable in lab. usually IGG usually EV.

61
Q

HDNF how it occurs

A

mother must be previously sensitized to antigen (previous pregnancy or transfusion). Baby must possess antigen. Mother must produce antibodies to this antigen that are capable of crossing placenta. Only IGG can cross placenta.

62
Q

ABO HDNF

A

An O mother has anti A and Anti B antibodies. A or B blood type in the fetus: IGG can cross placenta and case anemia even in first child,.

63
Q

billirunin in HDNF

A

mother conjugates and excretes in utero. After birth, remaining maternal antibodies still cause hemolysis. Infant is not efficient at metabolizing, and buildup of unconjugated can cause neurological defects.

64
Q

hdnf CLINICAL LAB FINDINGS

A

RETICULOCYTES CAN BE AS HIGH AS 60%. CORD BLOOD BILLIRUBIN IS ELEVATED.

65
Q

treatment for HDNF newborns

A

phototherapy: lowers billirubin in infants born with HDNF. Exchange transfusions: lowers billirubin, removes maternal antibodies, treats anemia.

66
Q

Rh Ig

A

injection of Rh ijmmunoglobulin prevents maternal immunization.

67
Q

Hemolytic Uremic Syndrome

A

hemolytic anemia with RBC fragmentation, thrombocytopenia, acute nepropathy renal failure. Seen in children. MOst common cause is from shiga toxin in ecoli. BUN and creatinine levels increased reflecting kidney damage.

68
Q

G6PD deficiency protects against

A

malaria. Could be more oxidants, early stage parasites more easily phagocytosed.

69
Q

G6PD sequence events pathophys

A

decreased NADH leads to oxidation of hb, and attachement of heinzbodies to band 3. Splenic macrophages pit and with progressive membrane loss sperocytes are formed. Spherocytes become trapped in the spleen.

70
Q

G6PD hemolysis usually caused by

A

exposure to oxidant drugs. Fava beans can also trigger. Primaquine (antimalarial).

71
Q

Hereditary non spherocytic anemia

A

is chronic. well compensated.

72
Q

blister cell

A

Hb oxidized and on one side of the cell. Indicative of oxidant related HA.

73
Q

Tests for G6PD deficiency

A

ascorbate cyanide test as screeening, quantitation at 340nm, molecular.

74
Q

PK clinical findings

A

autohemolysis increased at 48 hours, not corrected by glucose but corrected by ATP. Measure dissapearance of flourescence at 340 NM.

Hematology Module 2 (10 decks)

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