QUANTITATIVE RED CELL DISORDERS Flashcards

1
Q

develops due to inadequate intake, increased need, impaired absorption, and chronic blood loss

A

IRON DEFICIENCY ANEMIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

develops slowly, progressing through stages that physiologically blend into one another.

A

IRON DEFICIENCY ANEMIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Stage 1 IDA (Storage iron depletion)

Hemoglobin
Serum iron
TIBC
Ferritin

A

N
N
N

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Stage 2 IDA (Transport iron depletion)

Hemoglobin
Serum iron
TIBC
Ferritin

A

N


How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Stage 3 IDA
( Functional iron depletion)

Hemoglobin
Serum iron
TIBC
Ferritin

A




How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

IDA

A

Serum ferritin↓
Serum iron↓/N
TIBC↑
Transferrin saturation↓

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Thalassemia major

A

Serum ferritin ↑/N
Serum iron ↑/N
TIBC N
Transferrin saturation ↑/N

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

ACI

A

Serum ferritin ↑/N
Serum iron ↓
TIBC ↓
Transferrin saturation ↓/N

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Sideroblastic anemia

A

Serum ferritin ↑
Serum iron ↓/N
TIBC ↓/N
Transferrin saturation ↑

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Lead poisoning

A

Serum ferritin N
Serum iron - Variable
TIBC N
Transferrin saturation ↑

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

inflammation is the unifying factor

A

ANEMIA OF CHRONIC INFLAMMATION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

sideropenia in the face of an abundant iron stores is the central feature

A

ANEMIA OF CHRONIC INFLAMMATION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

the impaired ferrokinetics is the more significant cause of the anemia

A

ANEMIA OF CHRONIC INFLAMMATION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Substances that contribute/explain the inconsistency of decreased serum iron despite the abundant iron stores:

A
  1. Hepcidin
  2. Lactoferrin
  3. Ferritin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

a hormone produced by hepatocytes to regulate body iron levels

A

Hepcidin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

an iron-binding protein in granules of neutrophils

A

Lactoferrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

are a diverse group of diseases that include hereditary and acquired conditions

A

Sideroblastic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

the metal affects the central nervous system and the hematologic system

A

Lead Poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

interferes with porphyrin synthesis

A

Lead Poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

basophilic stippling is a classic finding

A

Lead Poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

represents punctate basophilia

A

Lead Poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

are diseases characterized by impaired production of the porphyrin component of heme

A

Porphyrias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

is the most often used to refer to the hereditary conditions that impair production of protoporphyrin

A

Porphyrias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

most common inherited porphyria

A

Acute intermittent hepatic porphyria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Deficient enzyme Uroporphyrinogen I synthetase/ Porphobilinogen synthase
Acute intermittent hepatic porphyria
26
Deficient enzyme Coproporphyrinogen II oxidase
Hereditary coproporphyria
27
Deficient enzyme Protoporphyrinogen oxidase/ Porphobilinogen oxidase
Variegate porphyria
28
Deficient enzyme Uroporphyrinogen decarboxylase
Cutaneous hepatic porphyria
29
Deficient enzyme Uroporphyrinogen III cosynthase
Congenital erythropoietic porphyria
30
Deficient enzyme Delta-aminolevulinic acid dehydrase and ferrochelatase
Acquired porphyria
31
Increased delta-aminolevulinic acid and porphobillinogen in urine
Acute intermittent hepatic porphyria
32
Increased coproporphyrin III in urine and feces
Hereditary coproporphyria
33
Increased porphobilinogen and delta-aminolevulinic acid in urine and protoporphyrinogen and coproporphyrin in feces
Variegate porphyria
34
Increased uroporphyrin I in urine
Cutaneous hepatic porphyria
35
Increased uroporphyrinogen I and coproporphyrinogen I in urine, feces, and bone marrow
Congenital erythropoietic porphyria
36
excess accumulation of iron results from acquired or hereditary conditions in which the body’s rate of iron acquisition exceeds the rate of loss.
IRON OVERLOAD
37
excess iron are stored in the form of ferritin and hemosiderin (non-metabolically active form of ferritin) within cells.
IRON OVERLOAD
38
Acquired iron overload
Transfusion-related hemosiderosis
39
accumulation of iron in the macrophages, with less parenchymal injury
Transfusion-related hemosiderosis
40
Hereditary iron overload
Hereditary hemochromatosis
41
mutations of HFE gene remain the most common
Hereditary hemochromatosis
42
individuals usually harbor 20 to 30 g of iron by the time their disease usually becomes clinically evident
Hereditary hemochromatosis
43
accumulation of iron in the parenchymal cells, with tissue injury
Hereditary hemochromatosis
44
traditional characterization of Hereditary hemochromatosis
Bronzed diabetes
45
Laboratory diagnosis of iron overload
Elevated transferrin saturation or serum ferritin Abnormal results on common tests of liver function
46
defective nuclear maturation due to impaired DNA synthesis due to Vitamin B12 or folate deficiency
MEGALOBLASTIC ANEMIA
47
the resulting DNA is nonfunctional, DNA replication process is incomplete, and cell division is halted
MEGALOBLASTIC ANEMIA
48
Example of ineffective erythropoiesis
Megaloblastic anemia
49
is an autoimmune disorder characterized by impaired absorption of vitamin B12 due to a lack of intrinsic factor
Pernicious Anemia
50
production of antibodies to intrinsic factor and gastric parietal cells
Pernicious Anemia
51
autoantibodies are directed against the a- and b- subunit of the gastric H+/K+ -ATPase, a hydrogen transporting enzyme, responsible for the acidification of the stomach lumen
Pernicious Anemia
52
caused by mutations in the genes for either cubilin or amnionless
Imerslund-Gräsbeck syndrome
53
Systemic manifestations of folate and vitamin B12 deficiency:
- general symptoms related to anemia - glossitis - gastritis, nausea, constipation - neurologic symptoms
54
Specific diagnostic tests Remains the reference confirmatory test to identify megaloblastic appearance of the developing RBCs
Bone marrow examination
55
Specific diagnostic tests Competitive binding chemiluminesence
Serum Vitamin B12
56
Specific diagnostic tests GC-MS
Methylmalonic acid
57
Specific diagnostic tests GC-MS, HPLC, FPIA
Homocysteine
58
Specific diagnostic tests Used to confirm achlorhydria
Gastric analysis
59
Specific diagnostic tests Chemiluminescent immunometric assay
Serum gastrin
60
Specific diagnostic tests Indirect fluorescent antibody techniques, ELISA
Parietal cell antibodies
61
Specific diagnostic tests Highly specific and confirmatory for pernicious anemia
Anti-IF antibodies
62
Is the metabolically active form of vitamin B12
Holotranscobalamin assay
63
Measures the ability of the marrow cells in vitro to utilize deoxyuridine for DNA synthesis
Deoxyuridine suppression test
64
Used to diagnose pernicious anemia
Schillings test
65
are macrocytic anemias in which DNA is unimpaired
Macrocytic nonmegaloblastic anemias
66
lack hypersegmented neutrophils and oval macrocytes in the peripheral blood and megaloblasts in the bone marrow
Macrocytic nonmegaloblastic anemias