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Clin Med I Exam #4 > 2 Anemia Part II > Flashcards

2 Anemia Part II Flashcards

1
Q

What factors can vary the clinical presentations of patients with anemia? (5)

A
  • Etiology
  • Severity
  • Onset (acute vs. chronic)
  • Age
  • Underlying condition of the patient
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2
Q

At what Hgb level do symptoms typically start becoming apparent in anemic patients?

A

Hgb < 10

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3
Q

Define Macrocytosis

A

RBCs are larger than usual size

MCV > 100

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4
Q

What can cause falsely elevated MCV levels? (2)

A
  • Large number of reticulocytes

- RBC clumping mimicking larger RBCs

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5
Q

Describe the disease process of megaloblastic anemia.

A

Defective DNA synthesis –> Disordered RBC maturation and accumulation of cytoplasmic RNA, reduced cell division –> Larger RBCs

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6
Q

Name the 2 types of Megaloblastic Anemia.

A
  • B12 deficiency

- Folate deficiency

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7
Q

What kinds of medications can cause drug-induced megaloblastic anemia?

A

Meds that interfere with purine and pyrimidine metabolism (AKA that inhibit DNA synthesis)

Examples:

  • Hydroxyurea
  • Chemotherapies
  • Antiretrovirals
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8
Q

What is the difference between folate and folic acid? Which one is more bioavailable?

A

Folate = dietary vitamin B9 (occurs naturally)

Folic Acid = synthesized vitamin B9, added to processed foods; more bioavailable!

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9
Q

What is the recommended daily intake of folic acid?

A

200-400 ng/day

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10
Q

Which foods provide dietary folate?

A
  • Fresh leafy veggies
  • Citrus fruits
  • Meat (beef, liver), Eggs
  • Fortified cereals, rice
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11
Q

Where does folate absorption primarily occur?

A

Jejunum

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12
Q

List some causes of nutritional folate deficiency (7).

Sorry these ones suck :-(

A
  • Alcoholism
  • Hemodialysis patients
  • Elderly patients
  • Toward the end of pregnancy
  • Anticonvulsant therapy (enzyme inhibition causes decreased folate absorption)
  • Malabsorption syndromes (rare)
  • Hemolytic anemias
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13
Q

What are the clinical features (symptoms) of folic acid deficiency?

A
  • Sx related to anemia (duh)
  • Glossitis
  • Vague GI sx
  • NO neurologic abnormalities!
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14
Q

A deficiency in WHAT can lead to neural tube defects during pregnancy?

A

Folic Acid!

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15
Q

What are the associated lab findings for Folic Acid Deficiency anemia?

A
  • Low serum folate level (<150 ng/mL)*
  • Elevated homocysteine level
  • Normal serum methylmalonic acid (MMA)*

*= different from B12 def. anemia (B12 and folate labs typically ordered together)

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16
Q

What will the peripheral smear show w/ Folic Acid Deficiency?

A

-Macro-ovalocytes
-Hypersegmented neutrophils
(very similar to a B12 smear)

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17
Q

What is the tx for folic acid def. anemia?

A
  • Replacement therapy
  • Treat any known underlying causes
  • Be sure to r/o coexisting B12 deficiency!!!
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18
Q

What is the ‘replacement therapy’ for folic acid deficiency?

A
  • 1 mg PO daily (use more in patients w/ malabsorption)

- Recommend taking with food for better absorption

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19
Q

Where do we get B12 from?

A

ONLY available from DIET

-Present in all animal products (meat, eggs, milk, etc.)

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20
Q

What is the primary cause of B12 def.?

A

Inability to absorb!

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21
Q

What is the recommended daily intake for B12?

A

1-2 ng

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22
Q

Between folic acid def. and B12 def., which of the stores runs out fastest? About how long does each take?

A
  • Folic acid = total body stores SMALL; anemia develops in 4-5 months w/ deprivation
  • B12 = body has LARGE stores; typically takes years to develop
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23
Q

List some causes of Vitamin B12 def. (5ish)

Sorry these ones suck :-(

A
  • Pernicious anemia (MOST COMMON!)
  • Decreased intake (freaking Vegans)
  • Medications (Metformin, H2 antagonists, PPIs)
  • Malabsorption (elderly)
  • Any condition which impairs B12 absorption (chronic gastritis, gastric surgery, ileal disease/resection, etc.)
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24
Q

What is pernicious anemia (PA)?

A
  • Auto-immune disorder caused by an immune mediated destruction/loss of gastric parietal cells
  • Results in IMPAIRED IF SECRETION!
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25
Q

What are some other associated issues with PA?

A
  • Accompanied by decreased gastric acid secretion
  • May be associated w/ other autoimmune diseases
  • Atrophic gastritis = Increased risk of gastric cancer
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26
Q

What is the clinical presentation/sx of a Vit B12 def?

A
  • Typical sx of anemia
  • Glossitis, stomatitis
  • GI sx
  • NEUROLOGIC AND/OR PSYCHIATRIC ISSUES*** Different from Folic Acid def!
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27
Q

What specific neurological sx can Vit B12 def cause? (4) How long are these sx reversible for?

A

Reversible if treated within 6 MONTHS of onset:

  • Decreased vibratory and position sense
  • Ataxia (abnormal gait)
  • Paresthesias (stocking-glove)
  • Confusion/dementia

Vit B12 def = defective myelin synthesis in CNS

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28
Q

What are the associated lab findings for Vit B12 Deficiency?

A
  • Elevated macrocytosis
  • Occasionally, leukopenia or thrombocytopenia
  • Low serum B12 levels***
  • Elevated Homocysteine levels AND elevated serum MMA levels***
  • If pernicious anemia present: Antibodies to IF and/or parietal cells + Increased gastrin
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29
Q

What will the peripheral smear show w/ Vit B12 Deficiency?

A

-Macro-ovalocytes
-Hypersegmented neutrophils
-Anisocytosis (size)
-Poikilocytosis (shape)
(very similar to folic acid def. smear)

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30
Q

What is the tx for Vit B12 def?

A
  • Parenteral Vit B12 (Daily IM/SQ injections of 1000ng for 1 week, THEN weekly injections for 1 month, THEN monthly injections for life)
  • Treat reversible causes
  • PO repletion for mild disease, depending on cause
  • Monitor potassium w/ tx
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31
Q

Why is it so important to differentiate between Vit B12 def and Folic Acid def (or both)?

A
  • Folate replacement will correct blood picture of Vit B12 def, BUT…
  • If Vit B12 also not replaced, pt may develop SERIOUS, POSSIBLY IRREVERSIBLE NEUROLOGICAL DAMAGE = “subacute combined degeneration of the spinal cord”
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32
Q

Describe the disease process behind hemolytic anemias.

A
  • Hemolysis = destruction of RBC
  • Hemolytic anemia = decreased RBC survival time
  • Bone marrow cannot compensate for RBC survival time of <20 days!
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33
Q

What are the clinical features of hemolytic anemia? (4)

A
  • Typical anemia sx
  • Jaundice
  • Gallstones (usually billirubin stones)
  • Dark urine
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34
Q

What are the lab findings for hemolytic anemia in general?

A
  • Anemia with increased reticulocyte count w/ polychromasia
  • Increased unconjugated bilirubin
  • Increase serum lactate dehydrogenase (LDH)
  • +/- hemoglobinuria/urine hemosiderin
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35
Q

What will the peripheral smear show w/ hemolytic anemia?

A
  • Immature RBCs
  • Nucleated RBCs
  • Schistocytes (fragmented RBCs)
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36
Q

What is a unique lab finding with intravascular hemoylsis HA?

A

Decreased serum haptoglobin

Binds Hgb released from lysed RBC = decrease free haptoglobin

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37
Q

Which test can we use to differentiate between the hemolytic anemias?

A

Direct antiglobulin (Coombs) test (DAT)

38
Q

Define extravascular hemoylsis (HA).

A

Destruction of RBCs in the reticuloendothelial system:

  • Spleen!!!!
  • Liver
  • Lymph nodes
  • Bone marrow
39
Q

What can the destruction of RBC in the reticuloendothelial system (ex: spleen) result in?

A

Extravascular hemolysis

40
Q

What disorder puts a patient at risk fro episodic hemolytic anemia?

A

-Pts with G6PD deficiency (x-linked recessive disorder)

41
Q

Why are pts with G6PD at risk for hemolytic anemia?

A

Deficiency of protective enzyme against oxidative stress = oxidative stress = episodic hemolytic anemia

42
Q

What are the oxidative stress triggers for pts with G6PD def?

A
  • Drugs: sulfa, antimalarials
  • Infections
  • Fava beans
43
Q

What are the clinical features of pts with G6PD def. related to hemolytic anemia?

A

No oxidative stress: asymptomatic, usually no splenomegaly

At times of episodic hemolysis:

  • Back or abdominal pain
  • Sx of anemia
  • Splenomegaly due to RBC sequestration
  • Jaundice
44
Q

What are the associated lab findings for G6PD def. related to hemolytic anemia?

A

MUST BE TAKEN DURING HEMOLYTIC EPISODE…

  • Increased reticulocytes
  • Increased indirect bilirubin
  • Low G6PD levels
45
Q

What will the peripheral smear show w/ a G6PD hemolytic episode?

A
  • Bite cells

- HEINZ BODIES (denatured Hgb)

46
Q

Tx for G6PD def. hemolytic episode?

A
  • Self-limited (resolves as RBCs are replaced)

- Avoid oxidative drugs

47
Q

What is hereditary spherocytosis? What does it do the RBCs?

A
  • Autosomal dominant disorder w/ mild hemolytic anemia
  • RBCs maintain normal MCV but have a smaller surface area
  • Have increased cell fragility (get trapped inside spleen then phagocytized by splenic macrophages)
48
Q

In regards to hereditary spherocytosis, what is different about patients who have undergone a splenectomy?

A

RBC life-span is normal (RBC life-span reduced if they still have a spleen)

49
Q

What are the clinical features/sx of hereditary spherocytosis?

A
  • Often asymptomatic; adapt well
  • May have mild jaundice/scleral icterus
  • Pigmented black gallstones!***
  • Splenomegaly
  • Chronic hemolysis creates need for increased folate (inadequate intake = megaloblastic anemia)
50
Q

What are the lab findings associated with hereditary spherocytosis?

A
  • Negative Coombs
  • Hyperchromic microcytosis
  • Osmotic Fragility test: RBCs demonstrate increased hemolysis on exposure to hypotonic fluid due to RBC membrane defect
  • RBCs are dense w/ globular appearance and lack central pallor
51
Q

What is the tx for hereditary spherocytosis?

A

SPLENECTOMY!

-Tx of choice for severe disease

52
Q

What is a risk for pts w/ hereditary spherocytosis undergoing a splenectomy? How can you help this?

A

Asplenia = increased risk of infection

  • Important to ensure they have appropriate pneumococcal vaccinations
  • Delay splenectomy until adulthood, if possible
  • Folate supplementation in the meantime
53
Q

What is sickle cell disease?

A

Autosomal recessive disorder which affects Hgb structure; RBCs become sickle shaped when deoxygenated, causing painful symptoms

  • Homozygous form: Hb SS = disease sx
  • Heterozygous form: HbS + HbA = carrier
54
Q

What are the signs/sx of sickle cell anemia in childhood?

A
  • Initial sx often swelling of the digits
  • Delayed growth and development
  • Usually starts at age 4-6 mos (Hgb F switching to adult Hgb)
55
Q

What type of infection can cause an aplastic crisis in a pt with sickle cell anemia?

A

Parvovirus B19 infection

56
Q

What are 3 hypoxic conditions that put patients with sickle cell anemia at risk?

A
  • Dehydration
  • High altitude
  • Intense exercise
57
Q

What are the clinical features of sickle cell disease?

A
  • Chronic hemolysis
  • Vaso-occlusive ischemic tissue injury
  • CHF, pulmonary HTN, dyspnea
58
Q

What can occur w/ chronic hemolysis in patients with SCD?

A

Aplastic crisis = sudden decrease in Hgb (life threatening!)

59
Q

What can occur w/ vaso-occlusive ischemic tissue injuries in patients with SCD?

A

-PAIN CRISIS (most common feature of this disease)
-ACUTE CHEST SYNDROME
^^^Know these 2 for sure. Can also have
-Osteonecrosis of femoral head and humeral head
-CVA, MI
-Splenic infarcts due to functional asplenia
-Skin ulcers (tibia common location)
-Renal infarcts resulting in inability to concentrate urine

60
Q

What are the lab findings associated with SCD?

A
  • Normocytic, normochrmoic anemia
  • Increased reticulocyte count
  • Thrombocytosis may be present
  • Hgb electrophoresis!!!! Reveals HbS
61
Q

What is the best test to confirm SCD diagnosis?

A

Hgb electrophoresis

62
Q

What will be seen on peripheral smear in patient with SCD?

A
  • A few sickled RBCs
  • Nucleated RBCs
  • Target cells
  • HOWELL-JOLLY BODIES (but not specific to SCD)
  • Thrombocytosis
63
Q

What is the tx for SCD?

A
  • Avoid precipitating factors
  • Analgesics, fluids, and O2 during pain crisis***
  • Hydroxyurea (chemo) to decrease incidence of painful crises***
  • RBC transfusions if needed
  • Vaccination against encapsulated organisms
  • Folate supplementation
  • Bone marrow transplant (only current curative tx)
64
Q

What is the cause of Autoimmune Hemolytic Anemia (AIHA)?

A
  • Autoantibodies adhere to surface of RBCs > Induce hemolysis
  • RBCs w/ Ag:Ab complex are phagocytized by macrophages > spherocytes formed > become smaller and are destroyed in the spleen
65
Q

What is the difference between primary vs. secondary AIHA?

A

Primary: No underlying systemic disorder
Secondary: Identifiable underlying systemic illness

66
Q

Name the 2 different autoantibodies that determine the clinical manifestations of AIHA?

A

IgM: Cold agglutinins
IgG: Warm agglutinins

67
Q

What are patients with AIHA at increased risk for?

A

VTE

68
Q

What are causes/associated conditions for AIHA? (6)

A
  • Autoimmune or connective tissue disorders (SLE, RA, etc.)***
  • Hematologic malignancy (CLL)***
  • Infection (Mycoplasma, EBV, HIV)
  • Immunodeficiency (prior organ/stem cell transplant)
  • Prior blood transfusion
  • Drugs
69
Q

What are the clinical features/symptoms of AIHA? (5ish)

A
  • Typical sx of hemolytic anemia (Pallor, jaundice, splenomegaly)
  • General: fevers, fatigue, weakness, dyspnea
  • Lymphadenopathy
  • Hemoglobinuria - dark urine
  • Acrocyanosis - dark purple to gray discoloration of fingertips, toes, or nose in exposure to cold
70
Q

What are the lab findings for AIHA?

A
  • Peripheral smear: Polychromasia, spherocytosis, and nucleated RBC
  • Positive Coombs (DAT) test (if RBC stick together = + test)
71
Q

What does tx of AIHA depend on?

A
  • Warm vs cold disease

- Age

72
Q

What is the tx for cold AIHA?

A
  • Cold does not typically need to be treated in most children (mild to self-limited)
  • Avoid cold exposure!!!
  • Rituximab
  • Plasmapheresis if necessary
73
Q

What is the tx for warm AIHA?

A
  • FIRST LINE: Corticosteroids!
  • Rituximab
  • Splenectomy
  • Immunosuppressants, IV immunglobin
74
Q

How does Rituximab (AIHA tx) work?

A

Ab that targets B cell lymphocytes

75
Q

What is intravascular hemolysis?

A

Destruction of RBCs within the blood stream

76
Q

What is fragmentation syndrome? What is seen on a peripheral smear?

A
  • Type of intravascular hemolysis caused by mechanical heart valve
  • Peripheral smear shows schistocytes (fragmented RBC)
77
Q

What causes a hemolytic transfusion reaction?

A

Abs to RBCs directed against the ABO/Rh blood grouping antigens
(RBCs attacked following transfusion)

78
Q

Along with a blood transfusion reaction, what else might cause a hemolytic transfusion reaction?

A

Hemolytic disease of the newborn (HDN) seen in erythroblastosis fetalis

79
Q

Which test can detect antibodies that coat a patient’s transfused RBCs?

A

Coombs test

80
Q

During what time period can a hemolytic transfusion reaction occur?

A
  • During or within 4 hours of transfusion

- Delayed rxns can occur up to 4 weeks later

81
Q

What are the sx of a hemolytic transfusion reaction? (8)

A
  • FEVER
  • Severe hypotension
  • Severe flank pain
  • Hemoglobinuria
  • Pain at infusion site
  • Chest tightness
  • DIC (oozing from IV site)
  • N/V/D
82
Q

What is paroxysmal nocturnal hemoglobinuria?

A

RARE acquired stem cell mutation resulting in complement mediate RBC lysis

83
Q

What are the clinical features of paroxysmal nocturnal hemoglobinuria?

A
  • Hemolytic anemia
  • Dark cola-colored urine at night/early AM w/ partial clearing during the day
  • Venous thrombosis of large vessels
  • Pancytopenia
84
Q

How do you dx paroxysmal nocturnal hemoglobinuria?

A
  • Flow cytometry
  • Osmotic fragility test
  • Coombs NEGATIVE
85
Q

What is the tx for paroxysmal nocturnal hemoglobinuria?

A
  • Monoclonal Ab against complement C5
  • Steroids
  • Stem cell transplant
86
Q

Describe aplastic anemia.

A

Acquired abnormality of hematopoietic stem cells

-May be total, or selective for RBCs, WBCs, or platelets

87
Q

What are the causes of aplastic anemia? (4)

A
  • 50% of cases are IDIOPATHIC***
  • Chemical/drug exposure (benzene, chloramphenicol, chemo)
  • Associated w/ viral illness (Epstein-Barr, cytomegalovirus, hepatitis)
  • Ionizing radiation
88
Q

What are the clinical features/symptoms of aplastic anemia? (5)

A
  • Pancytopenia is the hallmark!!! (anemia, leukopenia, thrombocytopenia)
  • Bone marrow: absence of precursors for normoblast, granulocyte, and megkaryocyte cells
  • Weakness
  • Infections
  • Bleeding
89
Q

What is the tx for aplastic anemia?

A
  • Bone marrow transplant = preferred tx! ***
  • Immunosuppressants if no BMT
  • ID cause, if possible, and treat it
  • Differentiate from other serious illnesses that may require different tx
  • Hematology referral
  • Transfusions as needed
90
Q

What are the causes of normochromic, normocytic anemias with INCREASED reticulocyte count? (2)

A
  • Prior or recent hemorrhage

- Recent acute hemolysis (as opposed to chronic hemoylsis)

91
Q

What are the causes of normochromic, normocytic anemias with NORMAL reticulocyte count and NORMAL bone marrow? (3)

A
  • Anemia of chronic disease
  • Hypothyroidism
  • Liver disease
92
Q

What are the causes of normochromic, normocytic anemias with NORMAL reticulocyte count and ABNORMAL bone marrow? (2)

A
  • Cancers: Myelofibrosis, leukemia, myeloma, metastases

- Renal failure

Clin Med I Exam #4 (7 decks)

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