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Summer 3 > Anemias > Flashcards

Anemias Flashcards

1
Q

What is on a CBC

A 
WBC 
differential 
RBC
Hgb
Hct
MCV
MCH
MCHC
Plt
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2
Q

What is normal RBC count

A

M: 4.7-6.1
F: 4.2-5.4
Normal lifespan: 120 days, then spleen eats them
RBC carry Hgb

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3
Q

What does Hgb do

A

bind and transport oxygen
M: 14-18
F: 12-16

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4
Q

What is the Hct

A

measure of % of total blood volume that is made up of RBC

Should be 3x the Hgb

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5
Q

What is the MCV

A

Volume determining average volume (size) of RBC
Normal: 80-100
Tells you micro vs macro vs normocytic

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6
Q

What is the MCH/MCHC

A

Avg mass of Hgb per RBC in a sample of blood. Less Hgb = less red. more Hgb = more red
Tells you hyper vs hypochromic

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7
Q

What is RDW

A

Red cell Distribution Width AKA measure of variation in size of RBC’s
Normal is 11-15%

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8
Q

What is anisocytosis

A

Increased variation in size of RBC

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9
Q

Increased RBC count can indicate

A

Dehydration
COPD (chronic hypoxemia)
Polycythemia vera

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10
Q

Decreased RBC count can indicate

A 
Anemia 2/2: 
bleeding
iron deficiency 
B12, folate deficiency 
hemolytic 
cirrhosis 
bone marrow failure 
pregnancy
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11
Q

What is anemia

A

Reduction in 1+ of major RBC measurements

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12
Q

What are reticulocytes

A

Immature RBC
Takes 1-2 days to mature
Indicate the bone marrow is producing RBC!
Normal: 1-2%

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13
Q

What is a pearl about recognizing reticulocytes in a peripheral smear

A

Lots of blue means Lots of new

Reticulocytes have a blue tint, and are larger than normal RBC

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14
Q

What are some causes of anemia

A

Impaired RBC production: iron, B12, folate deficiency, chronic disease, insufficient erythropoiesis
Increased RBC destruction: hemolysis
Blood loss: menses, GI, trauma, post-op

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15
Q

What are the characteristics of the different types of anemia*

A

Microcytic: small size, low MCV. Iron deficiency or Thalassemia
Normocytic: nl size, nl MCV. chronic disease
Macrocytic: large size, high MCV. Folate or B12 deficiency

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16
Q

How does anemia present clinically

A

Varies based on age, underlying condition, etiology, severity, and onset
Acute may have Sx even if mild
Chronic often doesn’t show Sx until Hgb <7!

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17
Q

S/Sx of anemia are

A 
Fatigue 
weakness 
light headed/ syncope
dyspnea 
palpitations 
pallor
tachy
hypotension
orthostatic changes 
\+/- heme in stool
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18
Q

Late signs of anemia are

A

Glossitis (big tongue)
Chelitis
Jaundice
Koilonichia

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19
Q

What is your differential for Microcytic anemia

A 
Iron deficiency (MC) 
Thalassemia 
Sideroblastic 
Lead poisoning 
-All with MCV <80
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20
Q

Common etiologies of iron deficiency anemia are

A

Menstrual blood loss
GI blood loss
Decreased iron absorption (celiac, bariatric surgery, H pylori infx)
Increased iron requirement (pregnancy)

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21
Q

Labs for Iron deficiency anemia will show

A 
Microcytic (MCV <80) 
MCHC is low 
RDW increased 
Ferritin <12 (low stores) 
Serum Fe is low 
TIBC is high 
Rarely need marrow Bx, but if you got it, it'd show absence of iron stores
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22
Q

What is Ferritin

A

an indicator of iron storage! If low, iron stores are depleted
Also an acute phase reactant! Will falsely elevate with acute illnesses

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23
Q

Clinical findings in iron deficiency anemia are

A

Glossitis, chelitis, koilonychia
Pica (cave ice, clay, dirt)
Dysphagia 2/2 esophageal webs (plummer vinson syndrome)
Restless leg syndrome

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24
Q

How do you treat iron deficiency anemia

A

ID and Tx cause**
R/o underlying occult malignancy
Replace iron stores (Ferrous sulfate 325 mg BID-TID until anemia corrects + 3-6 months after)
Blood transfusions (depending on Hgb), but not for iron replacement

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25
Q

What is thalassemia

A

inherited disorder MC affecting mediterraneans

Reduced synthesis of globin chains (alpha or beta)

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26
Q

What are the types of thalassemia

A

Alpha and Beta

Normally, you have 4 alpha and 2 beta chains per Hgb

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27
Q

How do alpha deletions affect manifestations of thalassemia

A

1 deletion: silent carrier

2: alpha thalassemia trait 2/ mild MICROcytic anemia
3: Hemolytic anemia
4: Hydrops fetalis

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28
Q

How does Beta thalassemia manifest

A

Minor (trait): dysfunction of one b chain. ASx, microcytic, hypochromic anemia
Major (Cooley’s anemia): severe dysfunction of both chains. Fatal if untreated

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29
Q

Thalassemia labs will show

A

MCV is low
Microcytic, hypochromic
RDW is normal
Iron is normal
Ferritin is high
Peripheral smear: Poikilocytosis (abn shape), Target cells*
Hgb electrophoresis helps Dx by detecting type of Hgb present

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30
Q

How do you treat thalassemia

A

Regular transfusions if severe +/- iron chelation therapy. AVOID iron supplementation
Folic acid supp.
Consider splenectomy
Hematopoietic stem cell transplant for severe B-thalassemia

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31
Q

What can falsely elevate MCV

A

Large number of reticulocytes (baby RBC)

RBC clumping together to mimic larger RBC

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32
Q

What are the types of macrocytic anemia

A

Megaloblastic: 2/2 abn cell division in RBC precursors (hypersegmented neutrophils)- B12 deficiency, folate deficiency
Non-megaloblastic: alcoholism, liver disease, reticulocytosis (hemorrhage, hemolysis)

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33
Q

Megaloblastic anemia is characterized by

A

Defective DNA synthesis
Disordered RBC maturation and accumulation of cytoplasmic RNA
Larger RBC

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34
Q

Info about Folate

A

Folic acid is in the diet
Need 200 mcg daily, 400-800 if regnant or trying to become
Half life: 3 weeks! total body stores are small
4-5 months deprivation causes macrocytic anemia
Absorption occurs in jejunum
Needed for DNA synthesis

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35
Q

Folate deficiency occurs in

A 
Alcoholism 
Hemodialysis 
Elderly 
End of pregnancy 
Anticonvulsant therapy (enzyme inhibition reduces folate absorption) 
Malabsorption syndromes 
Hemolytic anemia
36
Q

Clinical features of folic acid deficiency are

A

Sx related to anemia
Glossitis, vague GI Sx
NO neurologic abnormalities (but neural tube defects in baby)

37
Q

Lab findings for folic acid deficiency are

A

Low serum folate
Peripheral smear: Macro-ovalocytes, hypersegmented PMN
Homocysteine level elevated!! (methylmalonic acid is normal)

38
Q

How do you treat folic acid deficiency

A

Tx underlying cause (if known)
Replace 1mg PO, 5mg PO if w/ malabsorption
Rule out co-existing B12 deficiency!!

39
Q

Info about B12 (cobalamin)

A

Available from diet only
MCC is inability to absorb B12!
Need 1-2 mcg daily

40
Q

How is B12 absorbed

A

Taken in by diet
Binds IF in stomach (IF made by gastric cells)
Travels to small intestine together
Cobalamin is released in the jejunum where it is absorbed

41
Q

What conditions can cause B12 deficiency (impair the absorption)

A

Partial or complete gastrectomy (prevents IF secretion)
Ileal disease or resection
Bacteria overgrowth
Intestinal parasites

42
Q

What is pernicious anemia

A

Immune mediated atrophy of gastric parietal cells causing absent gastric acid and IF secretion
Autoantibodies against gastric parietal cells impair IF secretion
B12 deficiency that is AUTO IMMUNE

43
Q

Clinical features of pernicious anemia are

A

Typical anemia Sx
Glossitis, jaundice, splenomegaly
Atrophic glossitis, increased risk of gastric cancer
Neuro: Decreased vibratory and position sense, Ataxia, Paresthesias, confusion, dementia

44
Q

Lab findings in B12 deficiency and pernicious anemia are

A

High MCV
Leukopenia, thrombocytopenia
Periph: hypersegmented PMN, anisocytosis, poikilocytosis, macro-ovalocytes
Low serum B12
Elevated Methylmalonic AND homocysteine levels
+ Schilling test or Abs to IF (prenicious anemia)

45
Q

How do you treat pernicious anemia

A

Parenteral B12 (daily IM 100 mcg x 1 wk, then weekly for 1 mo, then monthly for life)

46
Q

How do you treat B12 deficiency

A

Supplement B12 PO

**NEVER treat B12 deficiency with Folate alone. this will mask a worsening PA and result in neurologic damage!

47
Q

What is hemolytic anemia

A

Decreased RBC survival time (20-100 days)

Can be compensated for by increased marrow production, but marrow can’t compensate for <20 days survival time!

48
Q

How do you classify hemolysis

A

Acute or chronic
Acquired or inherited
According to main site of hemolysis:
-intravascular: RBS destroyed in bloodstream
-extravascular: RBC destroyed in the spleen

49
Q

Lab findings in hemolytic anemia are

A

Elevated reticulocyte count (polychromasia)
Peripheral smear: immature RBC, nucleated RBC, +/- schistocytes (fragmented RBC)
Unconjugated bili increased
Elevated LDH

50
Q

What is Haptoglobin

A

Mucoprotein produced in the liver that binds Hgb released from lysed RBC
Will be low in intravascular hemolysis because it is binding all the lysed RBC Hgb

51
Q

Clinical features of hemolytic anemia are

A

Usual anemia Sx
Jaundice
Gallstones (bilirubin stones)
Increased risk of infection with salmonella and pneumococcus
Infection with ParvoB19 can cause transient aplastic crisis

52
Q

What can cause intravascular hemolysis

A 
Fragmentation syndromes (Macroangiopathic 2/2 trauma, Microangiopathis 2/2 RBC disruption from fibrin strand) 
Red cell enzyme deficiencies (G6PD deficiency) 
Paroxysmal nocturnal hemoglobinuria
53
Q

What is G6PD deficiency

A

X linked recessive disorder causing deficiency in G6PD, which is needed to keep RBC alive for full 120 days
Low G6PD= RBC undergo oxidative damage and precipitation of Hgb

54
Q

What can cause hemolysis in G6PD deficiency

A

Oxidative drugs= episodic hemolysis

Severe G6PD deficiency= chronic hemolysis

55
Q

Clinical features of G6PD deficiency are

A

Id episodic hemolysis, usually healthy with no splenomegaly

Women carriers rarely affected

56
Q

Lab findings in G6PD deficiency include

A

During hemolytic episodes: reticulocytes and serum indirect bilirubin increase
*Periph: Bite cells, Heinz bodies (denatured Hgb)
G6PD levels low

57
Q

How do yuo treat G6PD deficiency

A

Most cases are self limited

Avoid oxidative drugs

58
Q

What causes extravascular hemolysis

A 
Hereditary spherocytosis 
Sickle cell anemia 
AI hemolytic anemia 
Incompatible transfusion 
Drug induced hemolytic anemia
59
Q

What is hereditary spherocytosis

A

auto dominant d/o w/ mild hemolytic anemia
RBC have normal MCV, but smaller surface area. They are dense, round, and lack central pallor
They’re poorly deformable and get trapped in splenic sinusoids and are eaten by spleen macrophages
RBC lifespan is reduced if you have a spleen, and normal if you’ve had a splenectomy

60
Q

Clinical features of hereditary spherocytosis are

A

ASx (adapt well)
Mild jaundice/scleral icterus
Splenomegaly
Chronic hemolysis creates need for increased folate to avoid megaloblastic anemia

61
Q

Labs in hereditary spherocytosis are

A

Osmotic fragility test (RBC have increased hemolysis on exposure to hypotonic fluid)

62
Q

How do you treat hereditary spherocytosis

A

*Splenectomy! Restores nl RBC lifespan, removes risk of bilirubin gallstones
-Must give pneumovac 2/2 spleen cant fight off pneumococcal infection anymore
Wait to do splenectomy until adult, if possible

63
Q

What is Sickle cell disease

A

Autosomal recessive disorder where RBC contain HgbS under deoxygenated conditions
Homozygous= sickle cell disease (Sx)
Heterozygous= sickle cell trait (carriers, ASx)
MC in african american descent

64
Q

Clinical features of sickle cell disease are

A

Onset: In childhood (4-6 months) when fetal Hgb changes to adult Hgb
Delayed growth and development
Increased susceptibility to infections
Sx precipitated by dehydration, hypoxia, high altitude, intense exercise
Chronic hemolysis
Vaso-occlusive phenomenon

65
Q

What happens in chronic hemolysis (sickle)

A

Aplastic crisis= sudden decrease in Hgb
Bilirubin rises
May be life threatening!**

66
Q

What indicates a vaso-occlusive ischemic tissue injury (sickle)

A

Pain crisis (give fluids and analgesics)
Osteonecrosis of femoral and humeral heads
CVA, MI
Splenic infarcts causing fxnl asplenism
Leg ulcers

67
Q

What are lab findings in sickle cell disease

A

Hgb 5-11
RBC normochromic, normocytic
Elevated reticulocytes
+/- thrombocytosis
Hgb electrophoresis shows Hgb S (best confirmation test)
Periph: Howell-Jolly bodies*, target cells, nucleated RBC, few sickled RBC, thrombocytosis

68
Q

How do you treat sickle cell disease

A

Avoid precipitating factors (high altitude, dehydration, intense exercise)
RBC transfusions as needed
Analgesics, fluids, oxygen during crisis
Hydroxyurea*: decrease incidence of painful crisis by suppressing marrow fxn
Bone marrow transplant

69
Q

What is autoimmune hemolytic anemia (AHA)

A

caused by Abs that adhere to the surface of RBC and induce hemolysis by fixing complement and damaging cell membrane
RBC with Ag-Ab complex are phagocytized by macrophages and spherocytes are formed, that are destroyed by spleen

70
Q

What will labs for AHA show

A

Periph: Polychromasia, spherocytosis, nucleated RBC

+ Coomb’s test

71
Q

What happens with an incompatible blood transfusion

A

Most Abs to RBC are directed against ABO/Rh antigens

Incompatible blood results in hemolysis

72
Q

What is Coomb’s test

A

can detect Abs of patient coating transfused red cels

73
Q

What are the 3 blood transfusion reactions

A

Allergic
Febrile
Hemolytic

74
Q

How do you treat hemolysis

A

ID and Tx underlying cause
Corticosteroids
Splenectomy advised
Folic acid supplementation

75
Q

What is anemia of chronic disease

A

Can occur with Inflammation, organ failure, or in elderly
Caused by abnormal iron metabolism, impaired EPO production, or upregulation of hepcidin in response to inflammatory mediators

76
Q

Labs in anemia of chronic disease show

A

Normocytic, Normochromic
Nl-High ferritin
Variable serum Fe and TIBC (both low if inflammatory*)
Diagnosis of exclusion!

77
Q

How do you treat anemia of chronic disease

A

Treat underlying cause!

EPO may be beneficial

78
Q

What is myelodisplastic syndrome

A

Acquired disorder of hematopoietic stem cells characterized by dysplasia and cytopenia
Idiopathic or secondary
Mild-Severe
Dx: bone marrow biopsy*
May progress to marrow failure or leukemia*

79
Q

What is Sideroblastic anemia

A

Congenital or acquired RBC d/o
Inadequate marrow utilization of iron for heme synthesis despite normal iron levels being present
Bone marrow then produces ringed sideroblasts instead of healthy RBC

80
Q

What are ringed sideroblasts

A

Erythroblasts (precursor to RBC) with perinuclear iron engorged mitochondria

81
Q

What causes sideroblastic anemia

A 
*Myelodysplastic Syndrome 
Chronic alcoholism 
lead poisoning 
Meds 
Chronic infection or inflammation 
Malignancy
82
Q

Diagnostics for Sideroblastic anemia include

A 
MCV: low, normal, or high 
Moderate anemia (20-30%) 
Anisocytosis, Poikilocytosis 
Systemic iron overload* 
BM Bx: Ringed sideroblasts*, RBC may be stippled, blue stained iron , erythroid hyperplasia
83
Q

How do yu treat Sideroblastic anemia

A 
Tx underlying cause
Supportive Tx 
Tc iron overload if necessary (phlebotomy) 
Pyridoxine (B6) can help if CONGENITAL 
Acquired does not have a real cure 
Refer!
84
Q

What is aplastic anemia

A

Acquired abn of marrow stem cells, MC idiopathic

May be 2/2 drug exposure (benzene, chemo, chloramphenicol) or viral illness (EBV, CMV, hepatitis), or ionizing radiation

85
Q

Clinical features of aplastic anemia are

A

Pancytopenia*** (low Plt, RBC, WBC)
Bone marrow shows absence of precursors to all cells
Weakness, infections, bleeding

86
Q

How do you treat Aplastic anemia

A 
ID cause and eliminate it 
R/o other dz: acute leukemia, myelodysplasia, TB, etc.
Hematology referral 
*Bone marrow transplant*
Immunocuppressives if no transplant
87
Q

Associate buzz words

A

Target cells: thalassemia or liver disease
Rouleax formation: multiple myeloma
Heinz bodies: G6PD deficiency (aggregates of denatured Hgb)
Howell Jolly bodies: Sickle cell, spleen isn’t present or functioning
Smudge cells: CLL
Helmet cells: hemolytic anemias

Summer 3 (12 decks)

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