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Pathology 2 > Chapter 11- Hemolytic Anemias > Flashcards

Chapter 11- Hemolytic Anemias Flashcards

1
Q

Hereditary spherocytosis

Pathologic Cells

A

RBCs, destroyed via hemolysis

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2
Q

Hereditary spherocytosis

Patients

A

1:2,000 individuals from Northern European Ancestry

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3
Q

Hereditary spherocytosis

Unique Features

A

Autosomal dominant
mutations in RBC membrane proteins, weak RBCs are
removed by spleen, manifests with anemia & splenomegaly, jaundice, RBCs lack central pallor

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4
Q

Hereditary spherocytosis

Prognosis

A

Variable severity, most have minor anemia, possibly complicated by
parvovirus B19 infection (aplastic crisis), splenectomy may be Tx. for severely affected patients

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5
Q

Sickle cell anemia

Pathologic Cells

A

RBCs, destroyed by hemolysis

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6
Q

Sickle cell anemia

Patients

A

8% of African Americans are heterozygotes (trait), 1:600 are homozygotes (have anemia)

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7
Q

Sickle cell anemia

Unique Features

A 
Autosomal recessive betaglobin
mutation in the RBC
hemoglobin, makes RBCs
prone to thrombosis,
exacerbated by: blood is
sluggish (spleen, marrow),
dehydration, inflammation
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8
Q

Sickle cell anemia

Prognosis

A 
Heterozygotes are asymptomatic
and homozygotes express the
condition, 50% of homozygotes live
past their 50s, death is most
commonly from a stroke or acute
chest syndrome
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9
Q

α-thalassemia

Pathologic Cells

A

RBCs, destroyed

via hemolysis

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10
Q

α-thalassemia

Patients

A

Individuals from:
Mediterranean,
Africa, Southeast
Asia

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11
Q

α-thalassemia

Unique Features

A 
Both cause early RBC
hemolysis and damage RBC
precursors in marrow. 
α-thalassemia results from α-globin mutation and damages
RBCs due to unpaired β-globin
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12
Q

α-thalassemia

Prognosis

A

lethal in utero (4/4 mutations) or
asymptomatic carrier (1/4
mutations)

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13
Q

β-thalassemia (Minor/Major)

Pathologic Cells

A

RBCs, destroyed

via hemolysis

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14
Q

β-thalassemia (Minor/Major)

Patients

A

Individuals from:
Mediterranean,
Africa, Southeast
Asia

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15
Q

β-thalassemia (Minor/Major)

Unique Features

A

Both cause early RBC
hemolysis and damage RBC precursors in marrow. α-thalassemia results from α-globin mutation and damages
RBCs due to unpaired β-globin
(vice versa for β-thalassemia).

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16
Q

β-thalassemia
(Minor vs Major)
Prognosis

A

β-thal. minor: asymptomatic or
minor anemia, normal lifespan.

β-thal. major: severe, hair-on-end skull, growth restrictions, lethal
during 20s, hemochromatosis
(heart/liver failure) secondary to
repeated blood transfusion

17
Q

Glucose-6-phosphate
dehydrogenase (G6PD)
deficiency
Pathologic Cells

A

RBCs, destroyed

via hemolysis

18
Q

Glucose-6-phosphate
dehydrogenase (G6PD)
deficiency
Patients

A

Individuals from
Mediterranean or
the Middle East,
10% of U.S. blacks

19
Q

Glucose-6-phosphate
dehydrogenase (G6PD)
deficiency
Unique Features

A 
X-linked, RBCs are susceptible
to damage because
glutathione can’t be produced
without G6PD, hemolysis is
exacerbated by oxidants:
infections, aspirin, fava beans
20
Q

Glucose-6-phosphate
dehydrogenase (G6PD)
deficiency
Prognosis

A

Many patients are asymptomatic or
have very mild anemia, many go undiagnosed due to the lack of obvious features, avoidance of precipitating oxidants is
recommended.

21
Q

Paroxysmal nocturnal
hemoglobinuria (PNH)
Pathologic Cells

A

RBCs, destroyed

via hemolysis

22
Q

Paroxysmal nocturnal
hemoglobinuria (PNH)
Patients

A 
Individuals from
Southeast Asia or
the Far East,
frequently diagnoses
among middle-aged
adults
23
Q

Paroxysmal nocturnal
hemoglobinuria (PNH)
Unique Features

A

X-linked, PIGA gene mutations in myeloid stem cells, RBCs are susceptible to damage from complement fixation, which is exacerbated at night a pH drops slightly

24
Q

Paroxysmal nocturnal
hemoglobinuria (PNH)
Prognosis

A

This conditions is very rare, may be managed with antibodies that
inhibit the MAC of the complement system

25
Q 
Immunohemolytic anemias (Warm/Cold)
Pathologic Cells
A

RBCs, destroyed

via hemolysis

26
Q 
Immunohemolytic anemias (Warm/Cold)
Patients
A

Individuals with leukemia/lymphoma
and other or other
autoimmune disorders: SLE, RA, systemic sclerosis, or inflammatory bowel disease (Crohn, U.C.)

27
Q 
Immunohemolytic anemias (Warm vs Cold)
Unique Features
A

Opsonization of antibodies against one’s own RBCs, commonly results is removal of
RBCs in the spleen,
complement activation is also involved to a lesser degree
a) Warm: IgG, rarely IgA
b) Cold: IgM

28
Q 
Immunohemolytic anemias (Warm/Cold)
Prognosis
A

Mild-moderate anemia when the condition is isolated, may be associated with reduced lifespan in patients with serious comorbidities
(e.g. leukemia, SLE)

29
Q

Malaria (tertian malaria)

Pathologic Cells

A

RBCs, destroyed

via hemolysis

30
Q

Malaria (tertian malaria)

Patients

A

Anyone infected
with malaria:
Southeast Asia, Africa

31
Q

Malaria (tertian malaria)

Unique Features

A

Plasmodium falciparum
destroys RBCs as part of its lifecycle, merozoite showers every 48 hours, blackwater fever, fatigue, vomiting, jaundice, headaches, convulsions, loss of consciousness

32
Q

Malaria (tertian malaria)

Prognosis

A

Patient with malaria have a shortened lifespan and die from cerebral malaria, liver or kidney failure

Pathology 2 (7 decks)

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