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[Board Exam] Pathology > [4] Anemia > Flashcards

[4] Anemia Flashcards

1
Q

Definition of Anemia in Males and Females

A

Hb < 13.5 g/dL in Males

Hb < 12.g g/dL in Females

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2
Q

Based on MCV, anemia is classified as?

A

Microcytic: MCV < 80
Normocytic: MCV = 80 - 100
Macrocytic: MCV > 100

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3
Q

What is the progenitor RBC?

A

Erythroblast

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4
Q

Microcytic anemias are due to what defect?

A

Decreased production of Hb

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5
Q

Heme is composed of?

A

Iron and Protoporphyrin

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6
Q

Sideroblastic Anemia is due to?

A

Defective protoporphyrin synthesis

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7
Q

How do Thalassemias cause Microcytic Anemia?

A

Decreased production of globin chains

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8
Q

Most common type of anemia

A

Iron Deficiency Anemia

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9
Q

Absorption of heme occurs in what part of the GIT?

A

Duodenum

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10
Q

What is responsible for the uptake of iron in the gut?

A

Enterocytes

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11
Q

Iron is bound to this molecule in the blood

A

Transferrin

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12
Q

Storage sites for iron in the body

A

Liver and Bone Marrow

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13
Q

What does TIBC measure?

A

Amount of Transferrin in the blood

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14
Q

What does Serum Ferritin measure?

A

How much iron is in the storage sites

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15
Q

These parasites are common causes of iron deficiency

A

Necator and Ancylostoma (Hookworms)

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16
Q

How goes gastrectomy cause IDA?

A

Decreased acid would cause less iron to be in a reduced state (Fe 2+), which is better absorbed compared to Fe3+

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17
Q

RBCs in early stage Iron Deficiency Anemia present as?

A

Normocytic Anemia

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18
Q

Function: Hepcidin

A

Sequesters iron in storage sites

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19
Q

How does chronic disease cause iron deficiency anemia?

A

Release of acute phase reactants cause:

Hepcidin: Iron sequestration
Decrease of EPO production

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20
Q

What enzyme is the rate-limiting step for the production of Protoporphyrin?

A

Aminolavalunic Acid Synthase (ALAS)

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21
Q

What is the Co-Factor for the rate-limiting step for the production of Protoporphyrin?

A

Vitamin B6

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22
Q

Classic presentation of a RBC in Sideroblastic Anemia

A

Ring Sideroblast (Ring of Iron that is trapped inside the mitochondria)

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23
Q

Most common form of congenital Sideroblastic anemia is caused by?

A

Loss of ALAS

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24
Q

Common causes of Acquired Sideroblastic Anemia

A

Alcoholism: Mitochondrial poison damages the production of protoporphyrin

Lead Poisoning: Denatures ALAD and Ferrochelatase

Vitamin B6 Deficiency: Co-factor for the first step of Protoporphyrin production

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25
Q

Laboratory Findings in Patients with Sideroblastic Anemia

A

Ferritin: +
TIBC: -
Serum Iron: +
% Saturation Iron: +

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26
Q

Laboratory Findings in Patients with Iron Deficiency Anemia

A

Ferritin: -
TIBC: +
Serum Iron: -
% Saturation Iron: -

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27
Q

How do Thalassemias cause anemia?

A

Decreased synthesis of globin chains

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28
Q

Usual cause of alpha-thalassemias

A

Gene Deletion

Normally there are 4 Alpha Alleles are present on Chromosome 16

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29
Q

In an alpha-thalassemia, is a cis deletion or trans deletion worse?

A

Cis deletion (Same gene knockout)

Associated with increased risk of severe thalassemia in offspring

Usually seen in Asians

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30
Q

What is the pathophysiology that occurs in a 3 gene deletion alpha-thalassemia?

A

B chains may form tetramers that cause RBC damage

Patients present with severe anemia

31
Q

What is the pathophysiology that occurs in a 4 gene deletion alpha-thalassemia?

A

y chains form tetramers (Hb Barts) that damage RBCs

Fatal in utero (Hydrops fetalis)

32
Q

Beta-Thalassemia is caused by?

A

Gene Mutation (Not deletions like Alpha-thalassemias)

Two B genes are present on Chromosome 11, mutations result in absent (B0) or diminished (B+) production of B-globin chains

33
Q

What is the mildest form of Beta-Thalassemia?

A

B/B+ (Beta-Thalassemia Minor)

Usually asymptomatic with increased RBC count

34
Q

What is the most severe form of Beta-Thalassemia?

When does this disease present in the patient? Why?

A

B0/B0 (Beta-Thalassemia Major)

Presents with severe anemia a few months after birth because HbF (A2Y2) at birth is temporarily protective

35
Q

Treatment for patients with Beta-Thalassemia?

What is a complication of this treatment?

A

Chronic Transfusion

May cause secondary hemochromatosis (Remember that the body does not really have a way to remove iron)

36
Q

Presentation of Beta-Thalassemic RBCs on Blood Smear

A

Microcytic, hypochromic target cells with nucleated red blood cells

37
Q

Electrophoresis presentation of Beta-Thalassemia Major

A

HbA: - or 0
HbA2: +
HbF: +

38
Q

Most common cause of Macrocytic Anemia

A

Folate or Vitamin B12 Deficiency (Megaloblastic Anemia)

39
Q

How does folate or vitamin B12 deficiency cause anemia?

A

Impairs synthesis of DNA precursors

40
Q

What drug commonly causes macrocytic anemia?

A

5-FU

41
Q

Where is folate obtained from and where is it absorbed in the GIT?

A

Folate is obtained from green, leafy vegetables

Jejunum

42
Q

Blood smear finding of Macrocytic Anemia

A 
Macrocytic RBCs
Hypersegmented Neutrophils (>5 lobes)
43
Q

How does methylmalonic acid help differentiate a folate and vitamin B12 deficiency?

A

Normal serum levels of methylmalonic acid points to a folate deficiency as Vitamin B12 is necessary for its conversion to succinyl CoA

44
Q

In what part of the GIT is Vitamin B12 absorbed?

A

Ileum

45
Q

Why is Vitamin B12 deficiency less common than folate deficiency?

A

There is a large hepatic store of Vitamin B12

46
Q

Most common cause of Vitamin B12 deficiency

A

Pernicious Anemia

Autoimmune destruction of parietal cells leading to IF deficiency: Vitamin B12 binds to IF to be absorbed in the ileum

47
Q

How does pancreatic insufficiency cause B12 deficiency?

A

Lack of proteases to cleave the B12-R Factor unit, which prevents IF from binding to B12 for absorption

48
Q

What are reticulocytes?

A

Young RBCs released from bone marrow

49
Q

RBC Lifespan

A

120 Days

50
Q

How do you correct reticulocyte count?

A

Reticulocyte x Hct/45

51
Q

Define: Hereditary Spherocytosis

A

Inherited defect of RBC cytoskeleton membrane tethering proteins

Ankyrin, spectrin and band 3:1

52
Q

How does having a spherocyte shape of RBC cause anemia?

A

Unable to effectively pass through splenic sinusoids causing excessive destruction

53
Q

Diagnostic test for Hereditary Spherocytosis

A

Osmotic Fragility Test

Increased fragility in hypotonic solution

54
Q

Treatment for Hereditary Spherocytosis

A

Splenectomy

55
Q

What is a Howell-Jolly Body?

A

Histopathologic finding of remnant DNA in Erythrocytes usually seen in patients with severe splenic dysfunction

56
Q

What is the cause of Sickle Cell Anemia?

A

AR Mutation in B Chain of Hemoglobin

Glutamic Acid replaced by Valine

57
Q

What is the predominant Hb of Sickle Cell Anemia? What is the problem with this type of Hb?

A

HbS

These Hb polymerize when under oxidative stress causing the classic sickle pattern

58
Q

Treatment for Sickle Cell Anemia

A

Hydroxyurea

Causes increase of HbF, which is protective against sickling

59
Q

Most common cause of death for children with sickle cell anemia

A

Infection by encapsulated organisms (H. influenza, Strep pneumo)

Results from autophagy of the spleen

60
Q

Most common cause of death for adults with sickle cell anemia

A

Acute chest syndrome

Caused by vasoocclusion of pulmonary vasculature, usually preceded by an infection

61
Q

Cause of Hemoglobin C

A

AR defect of Hemoglobin B chain

Glutamic Acid is replaced by Ly-C-ine

62
Q

Pathophysiology of Paroxysmal Nocturnal Hemoglobinuria

A

Acquired defect in myeloid stem cells resulting in absent GPI

Renders cells susceptible to complement

(occurs at night due to mild respiratory acidosis that occurs during sleep)

63
Q

Screening Test for Paroxysmal Nocturnal Hemoglobinuria

A

Sucrose Test

64
Q

Confirmatory Test for Paroxysmal Nocturnal Hemoglobinuria

A

Acidified Serum Test

Flow Cytometry to detect lack of CD55 (DAF)

65
Q

In patients with G6PD Deficiency oxidative stress causes Hb to precipitate as?

A

Heinz Bodies

66
Q

What are some common causes of oxidative stress in patients with G6PD?

A

Infections
Drugs (Primaquine, sulfa drugs, dapsone)
Fava beans

67
Q

Presentation of patients with G6PD

A

Hemoglobinuria and Back Pain

68
Q

Pathophysiology of Autoimmune Hemolytic Anemia

A

IgG or IgM mediated destruction of RBC

69
Q

Treatment of Autoimmune Hemolytic Anemia

A

Cessation of offending drug
Steroids
IVIG
Splenectomy

70
Q

Test used to diagnose Immune Hemolytic Anemia

A

Coombs Test

71
Q

Which of the Coombs Tests are more important in the diagnosis of Autoimmune Hemolytic Anemia?

A

Direct Coombs: Anti-IgG is added to patients RBCs. If they are already coated with IgG, then they will agglutinate.

[Indirect Coombs: Tests whether the patients serum has the antibody]

72
Q

Hallmark of Microangiopathic Hemolytic Anemia

A

Schistoscytes

73
Q

Define: Myelophthisic Process

A

Pathologic process that replaces bone marrow resulting in pancytopenia

[Board Exam] Pathology (5 decks)

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