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Pathology - Blood Module > Hemolytic Anemia > Flashcards

Hemolytic Anemia Flashcards

1
Q

Common features of hemolytic anemia

A

Shortened life span of RBCs
Elevated erythropoietin levels
Accumulation of hemoglobin degradation products

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2
Q

__________ hemolysis is caused by alterations that render red cells less deformable.

A

Extravascular

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3
Q

Plasma haptoglobin levels ________ (increase/decrease) in hemolytic anemia

A

Decrease

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4
Q

__________ hemolysis is caused by mechanical injury, complement fixation, intercellular parasites (falciparum malaria) or exogenous toxic factors.

A

Intravascular

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5
Q

Free hemoglobin oxidises to ___________ if all haptoglobin is depleted

A

Methemoglobin

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6
Q

How does renal hemosiderosis occur in hemolytic anemia?

A

Hemoglobin and methemoglobin are reabsobed in the renal proximal tubule cells and catabolised there. Iron release from hemoglobin accumulate within tubular cells.

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7
Q

__________(increased/decreased) erythroid precursors (normoblasts) in marrow in hemolytic anemia

A

Increased

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8
Q

___________ hematopoiesis can appear in liver, sleen, lymph nodes (if anemia is severe)

A

Extramedullary

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9
Q

What are the clinical features of hemolytic anemia?

A 
Anemia
Hemoglobinemia
Hemoglobinuria
Jaundice (unconjugated bilirubin)
Gallstones (pigmented)
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10
Q

Lab investigations of hemolytic anemia

A 
CBC
Reticulocyte count
Serum LDH
Serum bilirubin (indirect)
Specific test
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11
Q

Serum LDH is __________ (increased/decreased) in hemolytic anemia

A

Increased

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12
Q

Hereditary spherocytosis is an autosomal _________ (dominant/recessive) disorder in 75% of the cases

A

Dominant

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13
Q

Life span of RBC in hereditary spherocytosis is ______

A

10-20 days

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14
Q

What happens in hereditary spherocytosis?

A

Intrinsic defects in red cell membrane skeleton that render red cells spheroid, less deformable and vulnerable to splenic sequestration and destruction.

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15
Q

Mutation weakens the interaction between these membrane skeleton proteins cause red cells to lose _______________

A

Membrane fragments

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16
Q

Young hereditary spherocytosis red cells are _________ (normal/spheoid) in shape

A

Normal

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17
Q

Membrane skeleton Proteins important for stability of the membrane include?

A

Ankyrin
Band 3
Spectrin
Band 4.2

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18
Q

Central pallor is 1/3 in normal red cells, but in hereditary spherocytosis the central pallor is ________ (high/absent)

A

Absent

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19
Q

Splenomegaly is found in ___________ hemolysis

A

Extravascular

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20
Q

What is aplastic crisis?

A

Bone marrow cannot make enough red blood cells

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21
Q

Aplastic crisis is triggered by ___________ which is transient

A

Acute parvovirus

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22
Q

What are the complications of hemolytic anemia?

A

Gallstones
Aplastic crisis
Hemolytic crisis

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23
Q

What are lab investigations of hereditary spherocytosis?

A

Family history
High MCHC
Osmotic fragility test

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24
Q

G6PD Deficiency is ___________ (Autosomal recessive/X-linked recessive) trait

A

X linked recessive

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25
There is ______ (trinucleotide-repeat/point) mutation in G6PD deficiency.
Point mutation
26
What occurs in G6PD deficiency?
Reduced ability of red cells to protect themselves against oxidative injuries and hemolysis occurs
27
Patients with G6PD deficiency have protective effect against ___________
Plasmodium falciparum malaria
28
Glucose 6 phosphate ———> ____________. The reaction is catalysed by enzyme Glucose 6 phosphate dehydrogenase
6 phosphogluconate
29
In the reaction involving G6PD, NADP+ is reduced to NADPH which helps to reduce ______ into GSH
GSSG
30
What are the clinical features of G6PD deficiency?
Neonatal jaundice Episodic anemia Dark colored urine Intravascular and extravascular hemolysis Older cells are much more susceptible to hemolysis than newer cells
31
Why older cells are more prone to hemolysis than younger ones?
Older cells have less deformability and less enzyme activity than younger cells
32
In G6PD deficiency, ________ (howell jolly/heinz) bodies are found in red blood cells.
Heinz bodies
33
How are Heinz bodies formed in G6PD deficiency?
Oxidants causes cross linking of reactive sulfhydryl groups on cloning chains, become denatured membrane bound precipitates
34
What are the lab investigations of G6PD deficiency?
``` CBC Peripheral blood smear Reticulocytosis Heinz bodies on supravital stain Methylene blue reduction test Hemoglobin in blood and urine Bite cells ```
35
Methylene blue reduction test is false negative in the case of __________
Acute hemolysis
36
ABO incompatibility results from ____ anti A and anti B and occurs in A or B group babies born to O group mothers
IgG
37
What are the lab investigations for mother in ABO incompatibility?
Test in mother 1. ABO and RhD grouping 2. Estimation of IgG antibodies in maternal serum
38
What are the lab investigations in infants with ABO incompatibility?
ABO and Rh typing Direct coomb’s test Serum bilirubin level (increased) Reticulocytosis (5%)
39
In Rh incompatibility, first pregnancy is ___________ (not affected/affected)
Not affected
40
Mother becomes sensitised against Rh positive during _________ (pregnancy/labor)
Labor
41
Kernicterous can occur in newborn if _____ incompatibility is severe
Rh
42
What are clinical manifestations of mild Rh incompatibility?
Anemia and jaundice
43
What are clinical features of moderate Rh incompatibility?
Hyperbilirubinemia (icterus gravis neonatorum, kernicterus)
44
What are the clinical features of severe Rh incompatibility?
Anemia develops in utero and intrauterine death
45
What are the symptoms of kernicterus?
Deafness Mental retardation Spasticity Neurological deficit
46
ABO incompatibility occurs in _______ (first/second) pregnancy
First
47
What are the investigations for mother in Rh incompatibility?
CBC Blood group Antibody screening and monitoring of levels
48
What are lab investigations for fetus in Rh incompatibility
Doppler ultrasound (middle cerebral artery systolic velocity) Chorionic villus sampling Amniocentesis Cordocentesis
49
Stillbirth and/or hydrops are frequent in ____ (Rh/ABO) incompatibility
Rh
50
Severe anemia is rare in ____ (ABO/Rh) incompatibility
ABO
51
Direct antiglobulin test is always positive in ____ (Rh/ABO) incompatibility.
Rh
52
There are no spherocytes present in ____ (Rh/ABO) incompatibility.
Rh
53
In _____ (Rh/ABO) incompatibility, exchange transfusion is frequently done.
Rh
54
What is the treatment of ABO incompatibility?
Phototherapy
55
What is the treatment of Rh incompatibility?
Exchange transfusion and phototherapy
56
Hemoglobin ___ is insoluble and forms crystal when exposed to low O2 tension
Hemoglobin S
57
There is a point mutation in the ___ (5th/6th/7th) codon of ______ (alpha-globin/Beta-globin) gene in sickle cell anemia
6th codon of the beta-globin chain
58
GAG which codes for glutamic acid is replaced by GTG that codes for _______ in sickle cell disease.
Valine
59
If both parents are heterozygous for sickle cell trait then Normal ____% Sickle cell trait ____% Sickle cell disease ___%
Normal 25% Sickle cell trait 50% Sickle cell disease 25%
60
What are pathological manifestations of sickle cell disease?
Chronic hemolysis Microvascular occlusions Tissue damage
61
In sickle cell trait, ____% of the hemoglobin is HbS
40%
62
Sicking occurs only under profound hypoxia in sickle cell _____ (trait/disease)
Trait
63
_____ inhibits the polymerization of HbS
HbF
64
After 5-6 months, infants develop sickle cells disease. Why is that?
HbF concentration decreases as the newborn grows and we know that HbF inhibits polymerization of HbS
65
Lysine is substituted for glutamate in the ____ (3rd/6th) amino acid residue of Beta-globin in _____ (HbS/HbC)
6th | HbC
66
In ________, cells lose salt and water and become dehydrated which leads to increased concentration of HbS in cells and increased polymerization of HbS
HbS-HbC
67
Microvascular beds with slow transit times _________ (increase/decrease) sickling.
Increase
68
Intracellular dehydration _________ MHCH, facilitate sickling
Increase
69
Homozygous HbS with alpha thalassemia _________ (increased/decreased) Hb synthesis that leads to milder disease
Decreased
70
A ________ (increase/decrease) in pH reduces the oxygen affinity of hemoglobin
Decrease
71
Low pH increases the fraction of ___________ (deoxygenated/oxygenated) HbS at any given oxygen tension and augmenting the tendency for sickling.
Deoxygenated HbS
72
HbS polymers herniate the red cell membrane leading to Influx of ______ Efflux of ______ and ______
Calcium influx | Potassium and Water efflux
73
Efflux of water 💦 causes dehydration in the RBCs leading to formation of __________
Sickle shaped RBCs
74
What is the Morphology of sickle cell disease
``` Irreversible sickled cells Howell jolly bodies Reticulocytosis Bone marrow is hyperplastic Skull resemble a crewcut Extramedullary hematopoiesis Pigment gallstones and hyperbilirubinemia ```
75
The term for red blood cells that are unequal in size is ___________
Anisocytosis
76
The term for red blood cells that are unequal in shape is ___________
Poikilocytosis
77
Howell jolly bodies is due to ______
Asplenia
78
______________occurs becuase infarcts are developed in spleen in sickle cell disease
Autosplenectomy
79
What is the vaso-occlusive crisis in sickle cell disease?
In bones of hip, lungs, spleen or brain | Hand-foot syndrome leading to variable length of fingers
80
What is Visceral sequestration crisis
Sickling within organs plus pooling of blood with anemia
81
Tx of sickle cell disease
Hydroxyurea | Allogenic transplant
82
Diagnosis of sickle cell disease
Blood smear Sickle solubility assay Hb electrophoresis High performance liquid chromatography (HPLC)
83
Blister cells and bite cells are seen in ____________ (hereditary spherocytosis/G6PD deficiency)
G6PD deficiency
84
In hereditary spherocytosis, 25% of the cases are _____________ (autosomal recessive/compound heterozygosity)
Compound heterozygosity
85
Why is MCHC is high in hereditary spherocytosis?
Dehydration caused by the loss of K and water from the red cells
86
``` What is more severe form of hereditary spherocytosis? Autosomal dominant Or Autosomal recessive Or Compound heterozygosity ```
Compound heterozygosity
87
What kind of mutations occur in hereditary spherocytosis?
Frameshift mutations or mutations that introduce premature stop codons so no membrane skeleton proteins are made.

Pathology - Blood Module (20 decks)

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