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X Clin Med Final > Anemia II > Flashcards

Anemia II Flashcards

1
Q

Limits of macrocytic anemia in adults and kids

A

Adults is an MCV>100

Kids is an MCV>90

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2
Q

Causes of macrocytic anemia

A

Reticulocytosis
Megaloblastic anemias
Liver disease/alcoholism, hypothyroidism, gastric bypass surgery

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3
Q

What are megaloblastic anemias?

A

Defective DNA synthesis results in disordered RBC maturation, accumulation of cytoplasmic RNA, reduced cell division in bone marrow and larger RBCs

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4
Q

Types of megaloblastic anemias

A

Folate deficiency
B12 deficiency
Drug-induced (drugs that interfere with pyrine/pyrimidine metabolism-hydroxyurea, chemotherapies and antiretrovirals)

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5
Q

Peripheral smear and bone marrow of B12 and folate deficiencies

A

They will be identical so must find another way to differentiate

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6
Q

Where do people get folate from?

A

The diet (vitamin B9)- usually food is supplemented with it

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7
Q

Daily allowance of folate

A

400 mcg (600 in pregnant and 500 lactating)

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8
Q

Symptoms of folate deficiency

A 
Anemia sxs duh
Glossitis (pain, swelling, tenderness, loss of papillae)
Vague GI symptoms
NO NEUROLOGIC SYMPTOMS
May see neural tube defects in pregnancy
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9
Q

Lab studies for folate deficiency

A

Decreased folate level

Increased homocysteine level and normal methylmalonic acid level

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10
Q

Treatment of folate deficiency

A

Treat the underlying cause again

Replacement therapy with folic acid: 1 mg PO daily and better absorbed with food

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11
Q

How does one get B12?

A

Only from diet (animal products)
1-2 micrograms a day
Deficiency usually develops over years because the body has large stores

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12
Q

How is B12 absorbed?

A

It is bound to intrinsic factor (gastric parietal cells) in the stomach and is then released from cobalamin-IF complex in ileum to be absorbed

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13
Q

What is the most common cause of B12 deficiency?

A

Pernicious anemia

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14
Q

What is pernicious anemia?

A

Deficiency of intrinsic factor that causes B12 malabsorption and megaloblastic anemia
There are autoantibodies against gastric parietal cells that impair IF secretion and gastric acid secretion
ITS AN AUTOIMMUNE DISORDER

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15
Q

Symptoms of pernicious anemia

A

Typical anemia sxs
Glossitis, jaundice, splenomegaly
Neurologic findings: decreased vibratory and position sense, ataxia, stocking-glove paresthesias, confusion, dementia, ataxia
Can be reversible if tx within 6 mos

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16
Q

What do you see on a peripheral smear in pernicious anemia?

A

Hypersegmented neutrophils (> 5 nuclear lobes)
Aniso and poikilocytosis
Macro-ovalcytes (large, oval RBCs)

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17
Q

Diagnostic tests in pernicious anemia

A

Decreased B12 level
+ Schilling test or antibodies to IF
Increased methylmalonic acid and homocysteine levels

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18
Q

Treatment for pernicious anemia

A

Daily IM/SQ injections of 1000 mcg B12 for 1 wk
Then weekly for a month and then monthly injections whole like
Treat reversible causes duh

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19
Q

What can happen when you treat B12 deficiency with folate?

A

Correcting the abnormal blood pic but the pt may develop serious, possibly irreversible neurological damage called subacute combined degeneration of the spinal cord

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20
Q

Cause of hemolytic anemias

A

Hemolysis of destruction of RBCs
Decreased RBC survival time (bone marrow can compensate with increased production when between 20-100 days but not below that)

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21
Q

Clinical presentation of hemolytic anemias

A

Anemia sxs
Jaundice
Gallstones (bilirubin stones)
Dark urine (Hb in urine)

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22
Q

Labs in hemolytic anemia

A 
Increased retic count
Increased UCB
Increased LDH
Decreased Hb
Hemoglocinuria/urine hemosiderin
Decreased haptoglobin in intravascular hemolysis
Direct antiglobulin (Coombs) test (DAT)
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23
Q

Best way to classify hemolytic anemias

A

According to site of RBC destruction:
Intravascular: in blood stream
Extravascular: in reticuloendothelial system (spleen)

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24
Q

Reasons for intravascular hemolysis

A

Shear stress: mechanical heart valve
Lysis from bacterial toxins: clostridial sepsis
Thrombotic microangiopathies: TTP, HUS
Red cell enzyme defects: G6PD def
Hemoglobinuria, transfusions, infections, snake bites

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25
Q

Random causes of intravascular hemolysis

A

Footstrike hemolysis or runners macryocytosis (runners), march hemoglobinuria (bongo drummers)

26
Q

What can you see with a mechanical heart valve?

A

Fragmentation syndrome, see shistocytes (broken RBCs)

27
Q

Reasons for extravascular hemolysis

A

Hereditary spherocytosis
Sickle-cell anemia
Thalassemias
Hereditary G6PD def

28
Q

Why is G6PD important?

A

Ensures normal lifespan of RBCs and is involved in the oxidizing process
Deficiency or unstable Hb leads to oxidative damage and precipitation of Hb

29
Q

What can oxidative drugs and infections do?

A

Cause episodic hemolysis (due to G6PD def)

30
Q

What do pts look like in a hemolytic episode?

A

Usually healthy with no splenomegaly

31
Q

Lab studies in G6PD deficiency

A

During an episode, reticulocytes and serum indirect bilirubin increase
Peripheral smear: Bite cells and Heinz bodies (denatured Hb)
G6PD low obvi

32
Q

Treatment for G6PD deficiency

A

Usually hemolytic episodes are self-limited when red cells are replaced
Do not use oxidative drugs!

33
Q

What is hereditary spherocytosis?

A

Autosomal dominant disorder with mild hemolytic anemia

34
Q

What happens to the RBCs in hereditary spherocytosis?

A

Normal MCV but smaller surface area (dense, globular appearance and lack central pallor)- SPHERE SHAPE
They are poorly deformable so get trapped in splenic sinusoids and taken in by splenic macrophages
RBC life span lower in ppl with spleen but not when have splenectomy

35
Q

Labs for hereditary spherocytosis

A

Osmotic fragility test: RBCs have increased hemolysis when exposed to hypotonic fluid due to RBC membrane defect

36
Q

Treatment of choice for hereditary spherocytosis

A

Splenectomy (restores RBC life span and removes risk of future bilirubin gallstones)

37
Q

What is the risk of splenectomy for hereditary spherocytosis?

A

Increases the risk of infections from encapsulated organisms so must have the right vaccinations and if possible, delay this until adulthood

38
Q

When is sickle cell anemia seen most?

A

African-American descent

39
Q

Most common feature of sickle cell anemia

A 
Pain crises:
Avascular osteonecrosis of femoral and humeral heads
CVA
MI
Splenic infarcts (asplenism)
Leg ulcers
40
Q

After when do you see sickle cell symptoms?

A

Dehydration, hypoxia, high altitude or intense exercise

41
Q

What are ppl with sickle cell at risk for?

A

Aplastic crisis and a sudden decrease in Hb

42
Q

What do you seen on a peripheral smear in sickle cell?

A

Sickled/nucleated RBCs, target cells, Howell-Jolly bodies (nuclear remnants usually removed by spleen)

43
Q

What is the best test to confirm sickle cell disease?

A

Hb electrophoresis (reveals the HbS)

44
Q

Treatment of sickle cell disease

A

RBC transfusions when needed
Hydroxyurea (chemo) to decrease incidence of painful crises (suppress bone marrow function of all cell lines)
Can try a bone marrow transplant

45
Q

What is autoimmune hemolytic anemia (AIHA)?

A

Immunologic destruction of RBCs mediated by autoantibodies directed against antigens on patients RBCs (clinical manifestations depend on the type of antibody produced)

46
Q

What is primary vs secondary AIHA?

A

Primary: no underlying systemic disorder
Secondary: identifiable underlying systemic illness

47
Q

What are people with AIHA at high risk for?

A

VTE

48
Q

Common associations with AIHA

A

SLE (and other autoimmune/connective tissue disease)
Hematologic malignancies
Etc.

49
Q

Clinical findings in AIHA

A

Sxs of hemolytic anemia
Fever and LAD
Hemoglobinuria
Acrocyanosis (dark purple to gray on fingertips, toes, nose in cold)

50
Q

First line tx for AIHA

A

Corticosteroids

51
Q

Other tx for AIHA

A

Depends if warm/cold disease and age (cold is usually self-limited in kids)
Rituximab: antibody to target B cell lymphocytes
Cytotoxic agents
Splenectomy

52
Q

When do you see a hemolytic transfusion reaction?

A

During or within 4 hrs of transfusion (can be up to 4 wks later but much less severe then)

53
Q

Common sxs of hemolytic transfusion reaction

A

FEVER, hemoglobinuria, hypotension, flank pain, pain at infusion site, chest tightness, N/V/D

54
Q

Why does hemolytic transfusion reaction occur?

A

Incompatible blood and severity correlates with the amount transfused

55
Q

Treatment for hemolytic transfusion reaction

A

Stop the transfusion obvi and treat with IVF, blood pressure support
Then submit a transfusion rxn work up

56
Q

What is aplastic anemia?

A

Immune injury of hematopoietic stem cells that may be life threatening (may be total or select for different blood components)

57
Q

Common causes of aplastic anemia

A

Most are idiopathic
Drugs/chemicals (benzene, chloramphenicol, chemo)
Viral illness (epstein-barr, cytomegalo, HBV)
Radiation
Genetic

58
Q

What are the features seen in pancytopenia?

A

Progressive anemia: weakness/fatigue
Neutropenia: recurrent infections
Thrombocytopenia: bleeding/hemorrhage

59
Q

What is the hallmark of aplastic anemia?

A

Pancytopenia (anemia, leukopenia, thrombocytopenia)

Bone marrow will not have precursors for those cells

60
Q

What is the preferred tx for aplastic anemia?

A

Bone marrow transplant (if can’t, then must do immunosuppressive therapy)

X Clin Med Final (5 decks)

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