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House Hemat > THE HAEMOLYTIC ANAEMIAS > Flashcards

THE HAEMOLYTIC ANAEMIAS Flashcards

1
Q

The life span of red blood cells is ____

A

120 days.

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2
Q

Haemolytic disorders are conditions which lead to a reduction in the _______ of red cells .

A

mean lifespan

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3
Q

↓in RBC lifespan →↑in rate of ________= compensated haemolytic state

A

erythropoiesis

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4
Q

When lifespan of RBC falls to _____, erythropoiesis can no longer compensate hence haemolytic anaemia ensues

A

15days

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5
Q

Haemolytic anaemia is therefore a form anaemia due to increased (premature) ___________, either in the ________(___) or _________(____) for which the ______ cannot compensate.

A

destruction of red blood cells (RBCs)

blood vessels (intravascular haemolysis)

elsewhere in the human body (extravascular)

marrow

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6
Q

HAEMOGLOBIN STRUCTURE

Hb molecule is a _____ of __ poly____ chains (globins),
A ______ molecule is attached to each globin chain.

A

tetramer; 4 ; peptide

haem

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7
Q

Adult Hb consist of
____ __chains , each ___ amino acid long
__ ___chains, each ____ amino acid long

A

2 α; 141

2 β ; 146

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8
Q

Hemolytic Anaemia Can be classified in several different ways:

Site of ______
Site of ______

A

destruction

defect

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9
Q

Hemolytic Anaemia Can be classified in several different ways:

Site of destruction*:
•_________ HA
•_________ HA

Site of defect**:
• __________ (______) defect
• _________ (_____) defect

A

Extravascular

Intravascular

Intracorpuscular; intrinsic

Extracorpuscular; extrinsic

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10
Q

Hemolytic Anaemia Can be classified in several different ways:

Site of destruction*:
• Extravascular HA: premature destruction of RBC by ______ in the _______
• Intravascular HA: haemolysis occur mainly in the _______

A

macrophages: Reticuloendothelia system (RES)

circulation

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11
Q

Hemolytic Anaemia Can be classified in several different ways:

Site of defect**:
• Intracorpuscular (intrinsic) defect: structural or functional defect ____ the RBC
• Extracorpuscular (extrinsic) defect: caused by abnormality in RBC’s _______

A

within

environment

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12
Q

CAUSES of INTRACORPUSCULAR (INTRINSIC) hemolytic Anaemia:

Inherited defects:

_______ defects
________ defects
__________

Acquired defects
___________

A

Red cell membrane
Enzymatic
Hemoglobinopathies

Paroxysmal nocturnal hemoglobinuria (PNH)

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13
Q

CAUSES of INTRACORPUSCULAR (INTRINSIC) hemolytic Anaemia:

Inherited defects
1. Red cell membrane defects
a. Hereditary _______
b. __________
c. Hereditary _______

A

spherocytosis

Pyropoikilocytosis

elliptocytosis

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14
Q

CAUSES of INTRACORPUSCULAR (INTRINSIC) hemolytic Anaemia:

Inherited defects:

Enzymatic defects

a. _____ pathway defects – _______ deficiency, etc.

b.______ pathway defects: ______ deficiency

A

Glycolytic; pyruvate kinase

Pentose; G- 6-PD

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15
Q

CAUSES of INTRACORPUSCULAR (INTRINSIC) hemolytic Anaemia:

Acquired defects
1. _____________

A

Paroxysmal nocturnal hemoglobinuria (PNH)

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16
Q

CAUSES of INTRACORPUSCULAR (INTRINSIC) hemolytic Anaemia:

Inherited defects: Hemoglobinopathies

a. Qualitative defects – ______ disease , _______ disease, _______ disease, etc.
b. Quantitative defects – _______

A

sickle cell
HB C
HB E

thalassemias

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17
Q

CAUSES of EXTRACORPUSCULAR (EXTRINSIC) hemolytic Anaemia :

_________ hemolytic anemias

__________ hemolytic anemias

A

Immune

Non- immune

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18
Q

CAUSES of EXTRACORPUSCULAR (EXTRINSIC) hemolytic Anaemia

Immune hemolytic anemias
_________
________

A

Auto- immune
Allo-immune

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19
Q

CAUSES of EXTRACORPUSCULAR (EXTRINSIC) hemolytic Anaemia

Non- immune

_______

________ agents

_______ processes
__________/_______

A

Infections

Physical

Microangiopathic

Splenic sequestration/hypersplenism

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20
Q

Microangiopathic processes include:

___________ (DIC), __________ (TTP), ___________ (HUS), etc.

A

disseminated intravascular coagulations

thrombotic thrombocytopenia purpura

hemolytic uremic syndrome

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21
Q

CLASSIFICATION OF HAEMOLYTIC ANAEMIA (HA)-

Inherited or acquired
– Typically, inherited disorders are caused by __________ defect
– Acquired haemolytic disorders are caused by ____________ factors

– Exceptions include:
________________

A

intrinsic (intracorposcular)

extrinsic (extracorpuscular)

Paroxysmal Nocturnal Haemoglobinuria (PNH)

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22
Q

Paroxysmal Nocturnal Haemoglobinuria (PNH) is an (inherited or acquired?) disorder with an (intrinsic or extrinsic?) defect.

A

Acquired

Intrinsic

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23
Q

Pathways of RBC Destruction: Extravascular

RBCs phagocytized by _____ cells
RBC ______ is broken down
Hemoglobin broken into ___________
___________ are recycled.

A

Reticuloendothelial

membrane

haem, iron and globin

Globin and iron

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24
Q

Iron binds to ______, returns to ______

Haem is broken down into _______

A

transferrin; marrow

excretable form

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25
Q

Pathways of RBC Destruction: Extravascular

Most hemoglobin degradation occurs within the ______ of the ____.

_____________ portions are conserved and reutilized.

Heme is reduced to _______, eventually degraded to _______, and excreted in the ____.

Thus, indirect indicators of erythrocyte destruction include the ______ level and _______ concentration in the _____.

A

macrophages; spleen

The globin and iron

bilirubin; urobilinogen; feces

blood bilirubin

urobilinogen; urine

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26
Q

Heme breakdown

Heme is (oxidized or reduced?) to ______ by _______ which is (oxidized or reduced?) by ______ to water (soluble or insoluble?) indirect ______ (conjugated or unconjugated?) which then binds to _____

A

Oxidized; biliverdin; heme oxygenase

Reduced; biliverdin reductase

Insoluble ; bilirubin; unconjugated

albumin

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27
Q

Indirect bilirubin is conjugated in the ____ by __________ to direct bilirubin which is water (soluble or insoluble?) capable of
______ and _____ excretion.

A

liver

glucoronly transferase

Soluble

biliary and renal

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28
Q

Haemolysis leads to excess production of bilirubin but within livers ability to conjugate

T/F

A

F

Beyond it

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29
Q

High plasma concentrations of unconjugated bilirubin (normal concentration ~ _____ mg/dL)

A

0.5

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30
Q

Pathways of RBC Destruction: intravascular

Free hemoglobin binds to _____ and is then (oxidised or reduced?) to ________ which binds to
–__________
– ________ :.
These proteins are cleared by the _____ where the heme is broken down to recover iron & produce bilirubin.

A

haptoglobin

Oxidized; methhemoglobin

hemopexin; albumin

liver

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31
Q

Methemoglobin + albumin = ______

A

methemalbumin

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32
Q

Pathways of RBC Destruction: intravascular

When the erythrocyte is destroyed within the vascular system, hemoglobin is released (directly or indirectly ?) into the ___. Normally, the free hemoglobin quickly complexes with _______, and the complex is degraded in the _____.

In severe hemolytic states, _____ can become depleted, and free hemoglobin dimers are __________

Additionally, with ______ depletion, some hemoglobin is quickly oxidized to _______ and bound to either _______ or _______ for eventual degradation in the liver.

A

Directly; blood

haptoglobin; liver

haptoglobin; filtered by the kidney.

haptoglobin; methemoglobin

hemopexin or albumin

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33
Q

CLINICAL FEATURES OF HAEMOLYTIC STATES

•Evidence of increased red cell destruction
–_______
–______

A

jaundice

pallor

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34
Q

CLINICAL FEATURES OF HAEMOLYTIC STATES

•Presence of ______ stones In chronic haemolytic states

•_______

•Expansion of _______ in (congenital or Acquired?) HA

– Frontal & parietal bossing

A

Pigment

Splenomegaly

marrow cavities

Congenital

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35
Q

EVIDENCE OF HAEMOLYSIS-

LABORATORY
Biochemical consequences of haemolysis
– Hyper_____________ (____jugated)
– Reduced ________

A

bilirubinaemia; unconjugated

serum haptoglobin

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36
Q

EVIDENCE OF HAEMOLYSIS-

Morphology:
Evidence of damaged red cells.

–_________, red cell ____,
________cells.

Evidence of increased red cell production
–________
– _______ red cells

Reduced red cell span
–____________ (____)

A

Micro-spherocyte; fragments; sickle

Polychromasia; Nucleated

Radioactive chromium (51Cr )

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37
Q

EVIDENCE OF HAEMOLYSIS-

CLINICAL:
______
______

A

jaundice
anaemia

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38
Q

EVIDENCE OF HAEMOLYSIS-

Intravascular haemolysis:

_________
Reduced serum __________
_______uria
________uria
Reduced _______ levels
_____________emia

A

Haemoglobinaemia

haptoglobulin

Haemoglobin

Haemosiderin

haemopexin

Methaemalbumina

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39
Q

Methaemalbuminaemia is tested for by the __________ test

A

Schumm’s

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40
Q

LABORATORY EVIDENCE OF
INCREASED ERYTHROPOIETIC ACTIVITY

•Peripheral blood:
-_________(polychromasia) and _________(nucleated red blood cells)
-_________ : high MCV

A

Reticulocytosis; erthroblastaemia

Macrocytosis

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41
Q

LABORATORY EVIDENCE OF
INCREASED ERYTHROPOIETIC ACTIVITY

•Bone marrow
-Erythroid ______
–Reduced _______/____ ratio

•Bone
Changes in the ______ and _____ bones

A

hyperplasia

myeloid/erythroid

skull and tubular

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42
Q

In extravascular hemolytic Anaemia, how is the :

Routine blood film
Reticulocyte count
Bone marrow examination
Bilirubin state in plasma or serum
Haptoglobulin levels in plasma or serum
Plasma hemoglobin

A

Polychromatophilia
Increased
Erythroid hyperplasia
Unconjugated
Reduced or absent
N or increased

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43
Q

In intravascular hemolytic Anaemia, how is the :

Routine blood film
Reticulocyte count
Bone marrow examination
Bilirubin state in plasma or serum
Haptoglobulin levels in plasma or serum
Plasma hemoglobin

A

Polychromatophilia
Increased
Erythroid hyperplasia
Unconjugated
absent
Very increased

44
Q

Presence of the following in the urine of a patient with intravascular hemolytic Anaemia

Bilirubin
Hemosiderin
Hemoglobin

A

No
Yes
Yes in severe cases

45
Q

Presence of the following in the urine of a patient with extravascular hemolytic Anaemia

Bilirubin
Hemosiderin
Hemoglobin

A

No
No
No

46
Q

COMPLICATIONS of hemolytic Anaemia

________ crisis
_________ in chronic haemolytic states

A

Aplastic

Leg ulcers

47
Q

TREATMENT of hemolytic Anaemia

Treat ____________

Give ________ especially in chronic haemolytic anaemia

May___________ in severe forms

A

the underlying cause

folic acid

require red cell concentrates

48
Q

RED CELL MEMBRANE Structure

___laminar, _____- dimensional

Outermost layer:______,_____
Central layer: _______,_______
Inner layer: _______

A

Tri; three

glycolipids, glycoproteins

cholesterol, phospholipids

cytoskeleton

49
Q

Hereditary sperocytosis

Defined as a group of hemolytic Anaemia characterized by the presence of (sparse or dense?), ______ shaped red cells without _____

A

Dense

spherically

central pallor

50
Q

Hereditary sperocytosis

The _________ renders it susceptible to premature removal by the _____

A

abnormal cell shape

spleen

51
Q

Most common congenital HA is ??

A

Hereditary sperocytosis

52
Q

Incidence of Hereditary sperocytosis is ????

A

1 in 5000

53
Q

Hereditary sperocytosis

Which is more severe between the autosomal dominant and autosomal recessive strain and by how much

A

autosomal recessive

25%

54
Q

Hereditary sperocytosis can be missed till adulthood

T/F

A

T

55
Q

In Hereditary sperocytosis l, Haemolysis is confined to the _____ and hence ____vascular

A

spleen

Extra

56
Q

MEMBRANOPATHY: Hereditary Spherocytosis

Complications:
- ______ crisis
- ________ anaemia
- _______ crisis
-________itis
-_________iasis
-_________

A

Aplastic

Megaloblastic

Haemolytic

Cholecyst

Cholelith

Severe

57
Q

MEMBRANOPATHY: Hereditary Spherocytosis

Differentials:

______ haemolytic anaemia
______ injury
_________reactions
hyper______

A

Immune
Thermal
Haemolytic transfusion
splenism

58
Q

Management of Hereditary Spherocytosis

– _______ 5mg weekly, ______ life long
– _________ in severe or complicated forms
–________ in severe hemolytic crisis

A

Folic Acid; prophylaxis

Splenectomy

Blood transfusion

59
Q

Hereditary Elliptocytosis is often symptomatic

T/F

A

F

Often aymptomatic(85%)

60
Q

In hereditary Elliptocytosis there is usually no splenomegaly

T/F

A

T

61
Q

In hereditary Elliptocytosis , Anaemia occurs

T/F

A

T

62
Q

Hereditary Elliptocytosis

Has 5 clinical syndromes:

_______
_____
______
______
______

A

slet carrier, common hemolytic Anaemia , HPP, spherocytic elliptocytosis and southeast Asian ovalocytosis

63
Q

most common enzyme defect of hemolytic Anaemia is ?

A

ENZYMOPATHY- G-6-Phosphate dehydrogenase deficiency

64
Q

ENZYMOPATHY- G-6-Phosphate dehydrogenase deficiency incidence is almost __% of the world’s population

A

1

65
Q

2 types of Normal G6PD enzyme

Most prevalent world wide is designated ___

About __% of healthy _______ have type __. Which has Normal enzyme activity

A

B

20

Africans

A

66
Q

G-6-Phosphate dehydrogenase deficiency is X linked

T/F

A

T

67
Q

G-6-Phosphate dehydrogenase deficiency is dominant

T/F

A

F

68
Q

G-6-Phosphate dehydrogenase deficiency

More common in males or females?

A

Males

69
Q

G-6-Phosphate dehydrogenase deficiency

The most common abnormal variant is the _____ type, designated ——–
– It is found in __% ____
– Enzyme activity is reduced to
About ____% of normal

A

African
A

10; blacks

10

70
Q

G-6-Phosphate dehydrogenase deficiency

Less common abnormal variant is the ______ type,
– Enzyme activity is reduced to ____%

A

Mediterranean

1- 3

71
Q

G-6-Phosphate dehydrogenase deficiency

Pathophysiology
– Red cell is protected from oxidative damage by constant regeneration of ____________ through the ________ cycle

-The continuous supply of ______ required to drive the ______ pathway is provide by the _________ pathway

A

reduced glutathione(GSH) via the glutathione cycle

NADPH; Hexose monophospshate

72
Q

G-6-Phosphate dehydrogenase deficiency
Patterns of haemolysis

– Chronic _________ HA

Life-long decompensated HA of variable severity which does not respond to ______

A

Non-spherocytic

splenectomy

73
Q

G-6-Phosphate dehydrogenase deficiency
Patterns of haemolysis

Episodic Haemolysis
• (More or Less ?) common presentation
• Acute haemolys is induced by increased _________- usually ____vasular Haemolysis

A

More

oxidant stress

Intra

74
Q

G-6-Phosphate dehydrogenase deficiency

• Triggers of acute haemolysis
– ______
–_____ beans- aaaaa
-_______

A

Drugs

Fava; favism

infections

75
Q

Triggers of acute hemolysis

Fava beans- favism

• Associated only with the ______ variance

A

Mediterranean

76
Q

• Most common cause of neonatal jaundice is ????

A

G-6-Phosphate dehydrogenase deficiency

77
Q

G6PD enzymes —activity—source

B
A
A-
M

A

100; widespread
90; blacks
8-20; blacks
0-7; Mediterranean whites

78
Q

Laboratory features of G6PD

–______
– ____ cells
-_____ bodies

A

Anisocytosis
Bite
Heinz

79
Q

IMMUNE HAEMOLY TIC ANAEMIA

Autoimmune HA:

• _________ hemolytic anemia

•_______ hemolytic anemia •
•____-induced IHA

A

Warm autoimmune

Cold autoimmune

Drug

80
Q

IMMUNE HAEMOLY TIC ANAEMIA

Autoimmune HA:

• Warm autoimmune hemolytic anemia
(Idiopathic, Secondary : ______ disorders, ______ diseases)

A

Lymphoproliferative; autoimmune

81
Q

IMMUNE HAEMOLY TIC ANAEMIA

Autoimmune HA:

• Cold autoimmune hemolytic anemia

-__________ syndrome
- _______________

A

Cold agglutinin

Paroxysmal cold hemoglobinuria

82
Q

Cold autoimmune hemolytic anemia

Cold agglutinin syndrome
• (Idiopathic, Secondary- _____, ________, LPD)
• Paroxysmal cold hemoglobinuria (Idiopathic, Secondary- _____,_____,_____)

A

mycoplasma; infectious mono

measles, mumps, syphilis

83
Q

IMMUNE HAEMOLY TIC ANAEMIA

Alloimmune HA
• As ________ reactions

A

blood transfusion

84
Q

Warm AI Hemolysis

Can occur at all age groups
T/F

A

T

85
Q

Warm AI Hemolysis is more common in which gender?

A

Female

86
Q

Warm AI Hemolysis is ____% idiopathic

A

50

87
Q

Cold AI Hemolysis
– Usually Ig ___
– Acute or Chronic form
– Chronic:

•C/F:
–______ patients
–____, ____ & often ___ fingers, toes, ears, or nose (_____)

•Inv:
– e/o hemolysis
– P Smear: Micro-spherocytosis
– Ig __ with specificity to ___ or ____

A

M

Elderly

Cold; painful; blue ; Acrocyanosis

M; I ; I Ag

88
Q

•
Treatment of Cold AI Hemolysis
– Treatment of the ______
– Keep _______
–_____ treatment
– Blood ______

A

underlying cause

extremities warm

Steroids

transfusion

89
Q

Treatment of Warm AI hemolysis

– Correct the underlying cause
–______ 1mg/kg po until Hb reaches ___mg/dl then taper slowly and stop
– ________: for life threatening problems
– If no response to steroids , try _______ or,
–__________: Azathioprine, Cyclophosphamide

A

Prednisolone

10

Transfusion

Splenectomy

Immunosuppressive

90
Q

NON IMMUNE HA

__________ to red cells

Drugs

______

Infections

Hyper______

A

Mechanical trauma

Burns

splenism

91
Q

NON IMMUNE HA
Mechanical trauma to red cells:

-Abnormalities in ________

  • ______________

-_____________ HA

A

heart and large vessels

March haemoglobinaemia

Microangiopathic

92
Q

NON IMMUNE HA
Mechanical trauma to red cells
•
Abnormalities in heart and large vessels
–
•
–
•
March haemoglobinaemia Burns
Aortic valve prostheses, coarctation of aorta Microangiopathic HA
Haemolytic uremic syndrome, thrombotic thrombocytopenia, disseminated intravascular haemolysis
–
•
• •
• Drugs
Infections
•
Malaria, clostridium perfringens
Hypersplenism

A
93
Q

Cold IHA; Warm IHA

AGE
Ig
Temperature

A

40-80; all age
M; G
3-4; normal body

94
Q

In cold, _____ clumps and activates _____

A

Rbc

IgM

95
Q

Dacrocyte is to ________ as drepanocyte is to _________

A

Myelofibrosis

Sickle cell

96
Q

Coombs test is positive in ????

A

Immune hemolytic Anaemia

97
Q

In G6PD deficiency

Favism is common in blacks of African Decent

T/F

A

F

98
Q

In G6PD deficiency

Morphologic findings include Heinz bodies, Blister Cell and bite cells

T/F

A

F

No blister cells

99
Q

Coomb’s tests is positive in only _____ Anaemia

A

Immune hemolytic

100
Q

Hb C disease is a genetic blood disorder that affects ______, a protein in red blood cells that carries oxygen. It is caused by a mutation in the ____ gene

In Hb C disease, the mutation results in the production of an abnormal hemoglobin called hemoglobin C. Hemoglobin C is _______ at carrying oxygen than normal hemoglobin (hemoglobin ___), which can lead to mild to moderate anemia.

A

hemoglobin

HBB

less efficient

A

101
Q

Thrombotic thrombocytopenic purpura (TTP)

caused by a deficiency or dysfunction of an enzyme called ______, which is responsible for _______ called _______.

Without this enzyme, VWF can accumulate in the blood vessels and form blood clots, which can block the flow of blood to organs and tissues.

A

ADAMTS13

breaking down a protein

von Willebrand factor (VWF)

102
Q

TTP is more common in which gender

A

Women

103
Q

hemolytic uremic syndrome

In all cases, HUS is characterized by the destruction of _______, the formation of _________, and ______ damage.

A

red blood cells (hemolysis)

blood clots in small blood vessels (thrombosis)

kidney

104
Q

Non-megaloblastic macrocytosis:

This type of macrocytosis is characterized by ____ red blood cells with _____ nuclei.

It can be caused by a variety of factors, including ____ disease, _______,_______ , certain medications (such as chemotherapy drugs), and ________ syndromes

A

large; normal

liver

alcoholism, hypothyroidism

myelodysplastic

105
Q

______ cells are seen in microandiopathic haemolysis

_________ are seen in autoimmune haemolysis

_________ are seen in hereditary spherocytosis

A

Fragment

Microspherocytes

Microspherocytes

106
Q

Presence of spherocytes in hemolysis caused by hereditary enzymopathies

T/F

A

F

House Hemat (29 decks)

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