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Medicine II > anemia > Flashcards

anemia Flashcards

1
Q

EPO is produced

A

by the kidney in response to adequacy of tissue oxygenation

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2
Q

role of EPO

A

enhances growth and differentiation of the erythroid progenitors into normoblasts

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3
Q

d. When a normoblast extrudes its nucleus to form a RBC it is called a

A

reticulocyte

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4
Q

Reticulocytes retain ribosomal network for about ____ and then

A

Reticulocytes retain ribosomal network for about 4 days (3 d in marrow, 1 d in blood) then lose RNA and become mature RBC

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5
Q

MCC of microcytic

A

i. IDA

ii. Thalassemia

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6
Q

MCC of normocytic

A

i. ACD (Anemia of chronic disease)

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7
Q

MCC of Macrocytic

A

i. B12/Folate deficiency
ii. With increased reticulocytes:
1. Hemolysis

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8
Q

sxs due to decreased oxygen or hypovolemia

A

Exertional dyspnea, dyspnea at rest, varying degrees of fatigue, bounding pulses, palpitations, “roaring” sound in the ears (can hear their heart beat in their ears)

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9
Q

e. Acute bleeding with severe volume depletion may lead to sxs of

A

fatigue, muscle cramps and can progress to postural dizziness, lethargy, syncope, hypotension, shock and death

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10
Q

mild anemia is more common with sxs associated with

A

exertion

as it progresses you will see fatigue and dyspnea at rest

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11
Q

PE and CM evidence for hemolysis

A

Splenomegaly
petechial rashes
jaundice abdominal pain = sign of hemolysis

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12
Q

evidence that the bone marrow is suppressed

A

Pancytopenia? Lack of retic count?

Recurrent infections

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13
Q

what do we want to start thinking of with iron deficiency

A

Why? lots of ETOH, dietary deficiency, underlying illness

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14
Q

NSAIDS and ASA

A

can cause bleeding and anemia

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15
Q

hydrourea

A

medication for sickle cell disease

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16
Q

worry about renal failure b/c

A

decreased EPO

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17
Q

LDA HSM and bonetenderness

A

can give you indication of underlying cancer or bone marrow probem

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18
Q

if your pt has anemia what would you expect from reticulocytes

A

high because if the bone marrow is healthy it should be pumping out more reticulocytes

if you have anemia the reticulocytes should NOT be 1% like it is normally

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19
Q

Iron studies/panel include

A

Iron, TIBC, transferrin saturation, ferritin

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20
Q

what to order if you suspect hemolytic anemia

A

LDH (elevated in certain types of CA and hemolytic anemia),

indirect bilirubin

haptoglobin (decreased in hemolytic)

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21
Q

why would you order EPO level or serum Cr

A

worried about anemia from renal damage

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22
Q

hypochromic microcytic anemia

A

IDA

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23
Q

Consider hemolysis in what type of anemia picture

A

normocytic

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24
Q

Leukopenia (low WBC) + anemia usually due to

A

bone marrow suppression, hypersplenism, vitamin B12 or folate deficiencies

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25
Q

Leukocytosis (increase WBC)+ anemia typically indicates

A

indicates infection, inflammation,

or hematologic malignancy (WBC over 60,000)

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26
Q

increase in neutriphils

A

iii. Inc neutrophils in infxn

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27
Q

; inc monocytes in

A

in myelodysplasia

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28
Q

inc eosinophils with

A

parasites or allergic disease

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29
Q

; dec neutrophils

A

s/p chemo

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30
Q

; dec lymphocytes

A

in HIV or steroid tx

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31
Q

Thrombocytopenia with anemia ddx

A

DDx includes

hypersplenism
malignancy involving bone marrow
autoimmune platelet destruction
sepsis
vitamin B12 or folate deficiency
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32
Q

Thrombocytosis with anemia ddx

A

DDx includes

myeloproliferative disease
chronic iron deficiency
inflammatory
infectious
 or neoplastic disorders
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33
Q

Can provide information not otherwise available in a CBC with diff

A

Peripheral blood smear

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34
Q

MCC on anemia

A

IDA

GIB is THE MCC of th MC anemia

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35
Q

Iron is stored primarily as

A

ferritin first levels to decrease with IDA

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36
Q

Causes of Iron Deficiency

A

¢ Deficient diet
¢ Decreased GI absorption
¢ Increased iron requirements (Pregnancy & lactation)
Blood loss (GI, menstrual, blood donation)
¢ Hemoglobinuria
¢ Iron sequestration (Pulmonary hemosiderosis)

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37
Q

pica is a sx related to

A

IDA

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38
Q

skin changes in anemia

A

” Skin and mucosal changes: smooth tongue, brittle nails, cheilosis (dry cracked areas on corners of mouth which can bleed)

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39
Q

if you have a clear suspicion of IDA or GIB

A

might have stool positive for a occult blood

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40
Q

first indicator of IDA

A

Ferritin

then TIBC due to increase binding sites open as iron is

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41
Q
  1. Peripheral smear from a patient with iron deficiency shows
A

pale small red cells with just a scant rim of pink hemoglobin; occasional “pencil” shaped cells are also present. Normal red cells are similar in size to the nucleus of a small lymphocyte (arrow);

thus, many microcytic cells are present in this smear. Thalassemia can produce similar findings.

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42
Q

tx of IDA

A

tx the cause and anemia

FeSO4 325mg PO TID = 1st line

Tana says she usually starts 1 time a day
also refer pts to dietician or council them on diet

don’t take iron with milk=bad absorption band constipation

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43
Q

MC SE of IDA tx

A

FeSO4 325mg PO TID

Causes nausea, constipation, dark stools in many pts

slow Fe or plant based iron less SE but —>less absorption

44
Q

when would you use parenteral iron therapy for IDA

A

” Intolerance to oral iron, refractory IDA, GI disease, uncorrectable continued blood loss

45
Q

when to recheck iron for IDA tx

A

3-6 mos after acheiving normal labs

should see return to H/H in 2 mos

want to check every 3 weeks or so until back to normal
then iron panel

want to keep checking periodically

46
Q

CC of anemia of chronic disease

A

Chronic infection or inflammation (Sarcoidosis, RA)
Cancer
Liver disease
Chronic renal failure

47
Q

pathophys of ACD

A

RBC survival is decreased

Bone marrow fails to compensate adequately for shorter RBC lifespan

48
Q 
o	↓ Serum ferritin 
o	↑ TIBC 
o	↓ Hgb/Hct
o	Microcytic, hypochromic cells
o	Anisocytosis & Poiklocytosis
A

Iron Deficiency Anemia (IDA)

49
Q

ACD is what type of anemia

A

normocytic anemia

50
Q

TX of ACD

A

” Treatment is not usually necessary
“ Purified recombinant erythropoietin is used in renal failure and some types of cancer or inflammatory diseases (eg: RA)
“ Hemodialysis is also used in patients with renal failure
“ Treat any coexistant iron or folate deficiency

51
Q

Thalassemias anemia is caused by defective

A

defective hemoglobinization of RBC

52
Q

hallmark of Thalassemias

A

Microcytosis out of proportion to the degree of anemia

53
Q 
o	↓ Hgb/Hct
o	↓ Serum iron, TIBC
o	↓ Serum EPO
o	Normocytic, normochromic cells
o	Normal retic count
o	↑/Normal serum ferritin
A

ACD

specifically in renal failure you will see decrease in EPO

low serum iron due to iron sequestering

going to see low TIBC

high ferritin

54
Q

Alpha-Thalassemia mainly effects

A

Affects primarily people from SE Asia and China

Alpha-Thalassemia

55
Q

Hemoglobin H disease is

A

Hemoglobin H disease is a severe form with excess β-chains that form a β4 tetramer

56
Q

type of thalassemia that is incompatible with life

A

Hydrops fetalis

57
Q

3 Alpha-globin genes

A

Silent Carrier Normal 80-100

58
Q

2 Alpha-globin genes

A

Thal. Minor 28-40% 60-75

these pts are completely fine with normal Hct and really marked MCV (60-72)

microcytsosis OUT OF PROPORTION

59
Q

1 Alpha-globin genes

A

Hgb H dz 22-32% 60-70

60
Q

α-thalassemia trait seen as what labs

how to dx

A

mild anemia
Hct 28-40%, very low MCV, normal RBC count

Reticulocyte count and iron studies normal

61
Q

CBC of Hemoglobin H Dz

A

marked hemolytic anemia, Hct 22-32%, very low MCV

Reticulocyte count is elevated

62
Q

Peripheral smear of α-thalassemia trait

A

microcytic, hypochromic RBC with

occasional target cells

63
Q

how to dx subtypes of alpha thalassemia

GOLD STANDARD

A

Hemoglobin electrophoresis shows no significant abnormality

64
Q

electrophoresis in Hemoglobin H Dz

A

Hemoglobin electrophoresis shows a fast migrating abnormal Hgb H as 10-40% of Hgb

65
Q

Hemoglobin H Dz Peripheral smear

A

hypochromia, microcytosis, target cells, poikilocytosis

66
Q

microcytosis out of proportion to anemia in italian or greek pt usually

A

Beta-Thalassemia

67
Q

Beta-Thalassemia usually Results in a relative increase in the percentage

A

Hgb A2 and Hgb F compared to Hgb A

68
Q

Beta-Thalassemia Major

A

Homozygous B

90-96% Hgb F

69
Q

Beta-Thalassemia Minor

A

Hgb A: 80-95%
Hgb A2: 4-8%
Hgb F 1-5%

70
Q

β-thalassemia minor (trait)

A

β-thalassemia minor (trait): clinically insignificant microcytic anemia

71
Q

when do we see sxs of β-thalassemia major

A

children normal at birth, develop severe anemia at 6 mos when Hgb F switches to Hgb A

72
Q

sxs of β-thalassemia major

A
  1. Growth failure, bony deformities, HSM, jaundice; requiring multiple transfusions
  2. If not treated properly, can develop cardiac failure, cirrhosis, endocrinopathies
73
Q

Peripheral smear from a patient with beta thalassemia trait.

A
  1. Peripheral smear from a patient with beta thalassemia trait. The field shows numerous hypochromic and microcytic red cells (thin arrows), some of which are also target cells (blue arrows).
74
Q

B-Thalassemia Major

A

tx with allogenic bone marrow transplant

Mild thalassemias do not usually require treatment

75
Q

” Hemoglobin H tx

A

disease treated with folate supplements and regular transfusions; iron chelation therapy often used; splenectomy

Mild thalassemias do not usually require treatment

76
Q

CBC of B-Thalassemia Major

A

severe anemia with very low Hct

77
Q

CBC of

B-Thalassemia Minor

A

” CBC: mild anemia, Hct 28-40%, MCV low (55-75 fL

78
Q 
Folic acid (folate) deficiency and c
yanocobalamin (vitamin B12) deficiency

are all

A

Megaloblastic Anemias

79
Q

Megaloblastic Anemias are macrocytic anemia seen with what smear

A
  1. Peripheral blood smear showing a hypersegmented neutrophil (7 lobes) and macro-ovalocytes, a pattern that can be seen with cobalamin or folate deficiency.
80
Q

with MCV elevation

A

check B12 AND foalte

81
Q

causes of B12 deficiencies

A

i. Decreased production of intrinsic factor

Pernicious anemia; gastrectomy

Helicobacter pylori infection

Competition for vitamin B12 in the gut

iv. Pancreatic insufficiency
v. Decreased ileal absorption of vitamin B12

Surgical resection; Crohn’s disease

Dietary and transcobalamin II deficiencies are rare causes

82
Q

tx for B12 deficiency

A

Pernicious anemia: 100mcg IM daily x 1 week then weekly x 1 month then monthly for life

1000mcg IM monthly (no PA)

” 1000mcg po qd continued indefinitely

83
Q

macrocytic anemia with neurologic findings

A

B12!!!!

84
Q

AFTER B12 tx when should pt return to normal

A
  • Hypokalemia may occur at onset of treatment

- Hematologic findings normalize in 2 months

85
Q

sxs of B12 macrocytic anemia

A

Changes in mucosal cells leading to glossitis; vague GI complaints including anorexia, diarrhea

Peripheral nerves affected leading to paresthesias, dysequilibrium, dementia and other neuropsychiatric changes

Reversible if treated within 6 months

Pale, mildly icteric; decreased position or vibration sense on PE

86
Q

dx studies for b12 deficient anemia

A

” Anemia of variable severity
“ MCV elevated to 110-140 fL
“ Peripheral smear with macro-ovalocytes, hypersegmented neutrophils; poikilocytosis and anisocytosis
“ Decreased reticulocyte count
“ WBC count and platelets may be decreased; pancytopenia may be present
“ Abnormally low serum vitamin B12 level

87
Q

Clinical Presentation of folic acid anemia

A

” Mucosal changes similar to vitamin B12 deficiency and megaloblastic anemia
“ No neurologic abnormalities
“ Symptoms of anemia
“ Fatigability, tachycardia, palpitations, DOE

88
Q

dx studies for folic acid anemia

A

” Anemia of variable severity
“ MCV elevated to 110-140 fL
“ Peripheral smear with macro-ovalocytes, hypersegmented neutrophils; poikilocytosis and anisocytosis
“ Decreased reticulocyte count
“ Decreased RBC folate or serum folate level
“ Normal serum B12 level

89
Q

causes of folic acid anemia

A

i. Dietary deficiency (lack of absorption)
1. Alcoholics, anorexia, malnutrition, overcook foods
ii. Decreased absorption
1. Tropical sprue; drugs (phenytoin, sulfasalazine)
iii. Increased requirement in –
1. Chronic hemolytic anemia; pregnancy; exfoliative skin disorders
iv. Loss of folic acid through dialysis
v. Inhibition of reduction to active form
1. Methotrexate

90
Q

general category for a decrease in RBC survival

A

XVI. Hemolytic Anemias

91
Q

Intrinsic RBC defects leading to hemolytic anemia

A

o Enzyme deficiencies
o Hemoglobinopathies
o Membrane defects

92
Q

Intravascular destruction of RBC leading to hemolytic anemia

A

o Microangiopathy
o Transfusion reactions
o Infections
o Paroxysmal hemoglobinuria

93
Q

Extrinsic RBC defects leading to hemolytic anemia

A 
o	Liver disease
o	Hypersplenism
o	Infections
o	Oxidant agents
o	Microangiopathy
o	Autoimmune 
o	Leukemia 
o	Burns
94
Q

most important tests for hemolysis

A

Decreased serum haptoglobin (won’t see this in other types of anemia)

Increased indirect bilirubin in the blood

also

Elevated serum LDH levels in microangiopathic hemolysis and others

Hemoglobinuria and positive urine hemosiderin with intravascular hemolysis

95
Q

Autosomal recessive hemoglobinopathy

A

Sickle Cell Anemia

Affecting 8% African Americans

96
Q

Factors that influence RBC sickling:

A

Concentration of Hgb S in the RBC –>the more Hgb S you have, the more likely you are to have sickling

RBC dehydration
Other types of Hgb in the cell (Hgb F)
 Anything that leads to deoxyhemoglobin state 1.	Acidosis, hypoexmia
97
Q

Sickle cell anemia c sickle cell trait

A

AS genotype in trait
40% Hgb S
SS in sickle cell
86-98% Hgb S

98
Q

Sickle cell crisis

A

Sickle cell crisis
“ Acute painful episodes due to acute vaso-occlusion; associated low-grade fevers
“ Clusters of sickled cells occlude the microvasculature of the organ(s) involved
“ Bones and chest most often affected
“ Last hours to days
“ Occur spontaneously or due to infection, dehydration, hypoxia

99
Q

Clinical presentation of sickle cell anemia

A

Chronic hemolytic anemia produces jaundice, pigment gallstones, hepatosplenomegaly

Poorly healing ulcers over the lower tibia, heart failure, retinopathy

Severe hemolytic or aplastic crises may occur when bone marrow decompensates or in splenic sequestration of sickled RBC

Chronically ill patients; poor growth and development

Life expectancy between 40-50 years of age

100
Q

Sickle cell diagnostic studies

A

Diagnostic Studies
“ Chronic hemolytic anemia with Hct 20-30%
“ Peripheral blood smear with sickled cells (5-50%), nucleated RBC, target cells, and Howell-Jolly bodies indicating hyposplenism
“ Reticulocytosis 10-25%
“ WBC count elevated 12-15K; thrombocytosis may occur
“ Increased indirect bilirubin b/c of hemolysis

GOLD STANDARD

Diagnosis confirmed by Hgb electrophoresis

101
Q

tx of sickle cell

A

No specific treatment is available for the primary disease of sickle cell anemia

Maintenance with folic acid supplements

Blood transfusions for aplastic or hemolytic crises

Acute crisis treated with oxygen, fluids, blood transfusion, and treatment of any underlying infection if present

Hydroxyurea (500-750mg/d orally) to reduce frequency of pain crises

Allogenic bone marrow transplant for young patients may be curative

Pneumococcal vaccination recommended to reduce infections, particularly post-splenectomy

102
Q

Very low MCV order

A

ii. Very low MCV order Hgb electrophoresis for thalassemias, SSD

103
Q

Normocytic usually

should order..

A

Usually ACD
order iron studies b/c these pts can have coexistent iron deficiency, CMP

Consider hemolysis, may need haptoglobin

104
Q

RBC Transfusion indications

A

10/30 Rule = Hgb < 10g/dL or Hct<30%

Estimated blood volume loss (>30%)

Symptomatic anemia (dizzy, SOB, fatigue)

105
Q

Effect of blood on H/H

A

Each unit of packed RBC (300mL volume has 200mL of RBC) will raise Hct 3-4% and Hgb 1g/dL if no continued bleeding

106
Q

Bone Marrow Biopsy indications

A

i. Unexplained anemia, leukopenia, thrombocytopenia, or pancytopenia
ii. Diagnosis/staging of lymphoma or solid tumors
iii. Diagnosis of plasma cell disorders and leukemia
iv. Evaluation of iron metabolism and stores
v. Evaluation of storage and deposition diseases
vi. Evaluation of FUO; suspected unusual infections
vii. Unexplained splenomegaly
viii. Evaluation of suspected chromosomal abnormality

107
Q

When to Refer

A

There appears to be more than one type or cause of anemia

A more complicated or unusual type of anemia is present

Anemia does not improve with treatment

Medicine II (21 decks)

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