Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Hematology > Hematology Week 1: Diminished Erythropoiesis > Flashcards

Hematology Week 1: Diminished Erythropoiesis Flashcards

1
Q

Hemolytic anemia Structural protein defects in one of these skeletal proteins

A
  • Ankyrin
  • Band 3
  • Spectrin
  • Band 4.2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

G6PD function

A

Important in making the reduced form of glutathione (GSH) which is critical in protecting against oxidant injury to the RBCs

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

G6PD Deficiency Genetics

A

X linked

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

G6PD Deficiency Triggers for hemolysis

3 listed

A

Infection - most common

Drugs - antimalarial

Food - Fava beans

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

G6PD Deficiency is most more common in? because?

A

Males because it is X-linked

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

G6PD Deficiency forms what kind of cells

A

Bite cells from the spleen removing precipitated Hb

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

Hemoglobin S AKA

A

Sickle Cell Disease

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

Most common hemoglobinopathy

A

Hemoglobin S (Sickle Cell Disease)

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

Hemoglobin S Mutation

A

Point mutation on Beta Globin gene leads to valine replacing glutamic acid at the 6th amino acid position

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

Hemoglobin S Prognosis​

A

Often leads to severe lifelong hemolytic anemia

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

Hemoglobin S etiology

A

Vascular obstruction -> tissue Infarction -> Sickle Cell Crisis

Hb will form tetramer and will not be flexible and will have difficulty traveling through the vasculature and the spleen

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

Hemoglobin S Diagonisis

A
  • Gold standard is hemoglobin electrophoresis
  • Identify HBS based on mobility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

β Thalassemia etiology

A
  • absent or reduced synthesis of β globin chains
  • increased α globin chains cause erythroid precursor damage
  • causing marrow expansion and extramedullary hematopoiesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

β Thalassemia Mutation

A

Due to >170 β gene mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

α Thalassemia

A

deletion of α gene resulting in a lack of α subunits and β subunits

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

α Thalassemia Mutations

A
  • Gene deletions are common
  • 2 deletions (asymptomatic mild anemia)
  • 4 deletions is fatal in utero (hydrops fetalis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

α Thalassemia genes

A

α 1 and α 2 on chromosome 16

so each person has 4 copies

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

Hydrops fetalis

A

α Thalassemia deletion of all 4 copies of α genes

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

α Thalassemia 3 copies deleted

A
  • soluble tetramers of β globins called H bodies
  • H bodies are minimally damaging to RBCs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Characteristic cell type of diminished erythropoiesis

A

Macroovalocytes

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

diminished erythropoiesis PBS findings

A
  • macroovalocytes
  • reticulocyte count is low
  • nucleated Red Cell Progenitors appear when anemia is severe
  • neutrophils are larger than normal and show nuclear hypersegmentation (macropolymorphonuclear)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Aplastic Anemia AKA

A

empty bone marrow

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

Myelophthisic Anemia

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

Question 1

A

B Kidney damage

because EPO is low despite anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Iron deficiency anemia

A

if you cant get enough iron you cant make enough Hb and you cant make as many RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Causes of iron deficiency

3 listed

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Impaired cytoplasmic maturation

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Polychromasia meaning

A

many colors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Peripheral smear of iron deficiency anemia

A

decreased RBC

reduced Hct

decreased Hb

Microcytic decreased MCV

hypochromic decreased MCHV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

CBC of iron deficiency anemia

A

decreased RBC

decreased HGB

Decreased HCT

Decreased MCV

Decreased MCHC and MCH

Increased RDW

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Iron absorption

A
  • Iron in the duodenum and ferroportin imports iron to blood stream
  • transferrin binds to iron and dleivers it to sotrage places of iron such as bone marrow and liver and is stored as ferritin
  • ferritin is used as the stored iron source for erythropoiesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Serum iron in iron deficiency anemia

A

Decreased

33
Q

Transferrin Iron Saturation in iron deficiency anemia

A

Decreased

34
Q

Total Iron Binding Capacity in iron deficiency anemia (TIBC)

A

Increased

35
Q

TIBC AKA

A

Total Iron Binding Capacity

36
Q

Ferritin in iron deficiency anemia

A

Decreased

37
Q

Bone Marrow Iron Stain

A

Prussian Blue Stain

38
Q

Laboratory portrait of iron deficiency

A
39
Q

Anemia of Chronic Disease

A
40
Q

Anemia of Chronic Disease arises in settings of?

A

Chronic Inflammation due to

  • infection
  • neoplasms
  • other sources of inflammation
41
Q

Anemia of Chronic Disease Purported mechanism

A

to deprive infectious organisms from getting iron for proliferation

42
Q

The most common cause of anemia in hospitalized patients

A

Anemia of Chronic Disease

43
Q

Chronic inflammations role in the absorption and processing of iron

A

Chronic Inflammation leads to production of many cytokines but particularly in this circumstance is the production of Hepcidin

Hepcidin blocks ferroportin and blocks the ability to use stored ferritin and decreases responsiveness to EPO

results in decreased production of RBC

44
Q

Hepcidin effects

4 listed

A
  • Hepcidin blocks ferroportin
  • blocks the ability to use stored ferritin
  • decreases responsiveness to EPO
  • reduces Erythropoiesis
45
Q

Serum Iron in Anemia of Chronic Disease

A

decreased

46
Q

Transferrin iron saturation in Anemia of Chronic Disease

A

decreased

47
Q

Total Iron Binding Capacity in Anemia of Chronic Disease

A

normal or decreased

48
Q

Ferritin in Anemia of Chronic Disease

A

normal or increased

49
Q

Laboratory portrait of in Anemia of Chronic Disease

A
50
Q

Why is anemia of chronic disease not microcytic and hypochromic?

A

usually, the responsiveness to EPO is the predominant effect

so basically not enough RBCs are being produced

51
Q

Failure of nuclear maturation cellular characteristics

A

macrocytic

52
Q

Pathway of DNA Synthesis

A

need to take folate to tetrahydrofolate (FH4) by methylating B12 into methyl-cobalamin

Methyl-cobalamin is restored to B12 by methylating homocysteine to methionine

B12 deficiency and Folate Deficiency decrease DNA synthesis

53
Q

B12 deficiency and Folate Deficiency cause?

A

B12 deficiency and Folate Deficiency decrease DNA synthesis

Megaloblastic anemia

54
Q

B12 deficiency leads to?

A

Megaloblastic anemia + demyelinating neurological symptoms

55
Q

Causes of vitamin B12 Deficiency

A
56
Q

Diphyllobothrium latum

A

Intestinal tapeworm absorbs B12 and competes for it

57
Q

Intestinal tapeworm absorbs B12 and competes for it

A

Diphyllobothrium latum

58
Q

How is vitamin B12 absorbed into the body?

A

R binder is secreted in saliva which binds to B12

Gastric parietal cells produce intrinsic factor

intrinsic factor binds to B12 after R binder is cleaved off

intrinsic factor receptors on intestinal epithelial cells bind to the B12+intrinsic factor complex absorbing it

59
Q

intrinsic factor Is produced by?

A

Gastric Parietal Cells

60
Q

Autoimmune attack to parietal cells causes

A

Pernicious Anemia

AKA

(B12 deficiency and megaloblastic anemia)

61
Q

Causes of Folate Deficiency

A
62
Q

How to differentiate Folate deficiency from B12 deficiency?

A

B12 increased homocysteine and increased methylmalonic acid-CoA

Folate Deficiency Increased homocysteine

63
Q

Folate Deficiency vs B12

A

Folate Deficiency Increased homocysteine only

64
Q

B12 deficiency vs folate deficiency

A

B12 increased homocysteine and increased methylmalonic acid-CoA

65
Q

Laboratory portrait of megaloblastic anemia with B12 and Folate indices

A

large RBC precursors (megaloblasts)

Macroovalocytes in the blood

hypersegmented neutrophils

66
Q

Megaloblastic anemia Histological features

A

large RBC precursors (megaloblasts)

Macroovalocytes in the blood

hypersegmented neutrophils

67
Q

Megaloblastic Anemia RBC#

A

low

68
Q

Megaloblastic Anemia Hb

A

Low

69
Q

Megaloblastic Anemia Hct

A

Low

70
Q

Megaloblastic Anemia MCV

A

High

71
Q

Megaloblastic Anemia RDW

A

High

72
Q

MCV as a tool for categorizing anemias

A
73
Q

Microcytic anemias examples

3 listed

A

Iron deficiency

Thalassemia

Lead poisoning

74
Q

Iron deficiency anemia treatment

A

Oral or IV (Oral is not tolerated well by many patients) (GI issues)

must identify the cause of the deficiency

remember Occult GI bleeding due to undiagnosed colon cancer

75
Q

Iron Deficiency Anemia Caveat

A

remember Occult GI bleeding due to undiagnosed colon cancer!

76
Q

Anemia of Chronic Disease treatment

A

Treat underlying condition

(+/- erythropoietin injection)

(+/- RBC transfusion)

77
Q

Megaloblastic Anemia Treatment

A

Supplementation of B12 (Oral or Intramuscular) or folate (Oral or IV)

DONT CONFUSE THESE CAN MAKE PATIENT WORSE!

78
Q

Megaloblastic Anemia Caveat

A

Be Careful don’t mix up folate deficiency from B12 deficiency

the folate might lessen the anemia but can make the neurological symptoms worse

Hematology (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions