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Anemia 2 Flashcards

1
Q

lab findings for folic acid deficiency

A

low serum folate level <150
-peripheral smear: macro-ovalocytes
**homocysteine level is elevated, but serum methylmalonic acid MMA is normal
(both would be elevated in B12 deficiency)

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2
Q

folic acid deficiency treatment

A

treat underlying cause
replacement therapy 1mg PO daily (better with food)
(be sure to rule out coexisting B12 deficiency)

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3
Q

average daily requirement of folic acid

A

200-400 micrograms/day

increase to 400-800 micrograms/day for pregnant, breastfeeding, or trying to conceive

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4
Q

most common cause of vit B12 deficiency

A

inability to absorb B12

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5
Q

the process of vit B12 absorption

A
  • vitamin B12 is bound to intrinsic factor (IF) in STOMACH
  • IF is produced by gastric parietal cells
  • B12 is released from cobalamin-IF complex in the ILEUM where it is absorbed
  • B12 is stored in the liver
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6
Q

vitamin B12 deficiency etiology

A
  • pernicious anemia (most common)
  • decreased dietary intake (vegan diet)
  • medications (metformin, H2; antagonists, PPIs)
  • malabsorption (elderly)
  • any condition which impairs absorption such as chronic gastritis or gastric surgery, ileal disease or resection, bacteria overgrowth or intestinal parasites, pancreatic insufficiency
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7
Q

What is pernicious anemia

A

caused by an immune-mediated destruction/loss of the gastric parietal cells -> impaired IF secretion

  • PA is an autoimmune disorder
  • low gastric acid secretion
  • atrophic gastritis leads to increase in gastric cancer
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8
Q

vit B12 clinical features

A

typical signs of anemia

  • glossitis
  • stomatitis
  • GI symptoms

Neurologic

  • decrease vibratory and position sense
  • ataxia
  • paresthesias (stocking-glove)
  • confusion/dementia

DEFECTIVE MYELIN

symptoms are reversible

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9
Q

vit B12 deficiency lab findings

A
  • increase macrocytosis MCV
  • occasionally: leukopenia, thrombocytopenia
  • peripheral smear: hypersegmented neutrophils (greater than or equal to 5 nuclear lobes), anisocytosis (size), poikilocytosis (shape), macro-ovalocytes
  • decrease serum B12

Pernicious anemia: antibodies to IF and/or parietal cells, Increase gastrin

Elevated serum methylmalonic acid and homocystein levels

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10
Q

Treatment of vitamin B12 deficiency

A
  • parenteral vit B12
  • daily IM/SQ infections of 1000 micrograms for 1 week
  • then, weekly injections for 1 month
  • then, monthly infections for life

treat reversible causes such as Diet, meds, SIBO, pancreatic insufficiency

  • PO repletion for mild disease, depending on cause
  • monitor patassium with treatment

-DO NOT TREAT WITH FOLIC ACID ALONE -> can cause irreversible neurological damage called subacute combined degeneration of the spinal cord

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11
Q

where can you find vit B12

A

meat, milk, eggs

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12
Q

hemolytic anemia

A

decrease in RBC survival time 20-100 days vs normal 120

marrow cannot compensate for RBC survival time <20 days

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13
Q

Clinical features of hemolytic anemia

A
  • typical anemia symptoms
  • jaundice
  • gallstones
  • dark urine
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14
Q

hemolytic anemia lab findings

A

-INCREASED RETICULOCYTE COUNT, POLYCHROMASIA (bluish)

Peripheral smear

  • immature RBCs, nucleated RBCs
  • schistzocytes (fragmented RBCs)
  • increased unconjugated bilirubin increased
  • increased serum lactate dehydrogenase (LDH)
  • decreased serum hepatoglobin in intravascular hemolysis

-Direct antiglobulin (coombs) test (DAT) can help distinguish between hemolytic anemias

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15
Q

Extravascular hemolysis

A
  • Destruction of RBCs in the reticuloendothelial system
  • spleen
  • liver
  • lymph nodes
  • bone marrow
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16
Q

G6PD deficiency

A

G6PD deficiency can cause chronic hemolysis

Deficiency of protective enzyme + oxidative stress = episodic hemolytic anemia

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17
Q

What can cause oxidative stress

A
  • drugs: sulfa drugs, antimalarials
  • infections
  • fava beans
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18
Q

G6PD deficiency clinical features

A

pts with episodic hemolysis are usually asymptomatic except during times of oxidative stress

  • usually no splenomegaly
  • x-linked recessive disorder
  • female carriers rarely affected
  • back or abdominal pain
  • symptoms of anemia
  • splenomegaly due to RBC sequestration
  • jaundice
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19
Q

G6PD lab findings

A 
During hemolytic episodes, reticulocytes and serum indirect bilirubin increase 
-peripheral smear:
bite cells
heinz bodies (denatured hemoglobin)
-G6PD levels will be low
20
Q

treatment of G6PD deficiency

A
  • most cases of hemolytic episodes are self-limited as red cells are replaced
  • oxidative drugs should be avoided
21
Q

What is hereditary spherocytosis

A

autosomal dominant disorder with mild hemolytic anemia
-intrinsic defect in the RBC membrane/cytoskeleton

  • RBCs are poorly deformable -> get trapped in the splenic sinusoids -> phagocytized by splenic macrophages
  • increased cell fragility
  • RBC lifespan is reduced in pts with a spleen and normal in patients who have had a splenectomy
22
Q

hereditary spherocytosis clinical freatures

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
23
Q

hereditary spherocytosis lab findings

A

-test = osmotic fragility test
RBCs demonstrate increased hemolysis on exposure to hypotonic fluid due to RBC membrane defect
-hyperchromic micirocytosis
-coombs NEGATIVE

24
Q

hereditary spherocytosis treatment

A

-SPLENECTOMY is treatment of choice (restores RBC lifespan to normal, removes risk of future bilirubin gallsotones)

-asplenia increases risk of infection from encapsulated organisms like pneumococcus so:
ensure appropriate vaccination pneumococcal
delay splenectomy until adulthood if possible
folate supplementation in meantime

25
what is sickle cell
- hereditary disorder of hemoglobin structure, transmitted through an autosomal recessive gene - Homozygous form Hb SS: sickle cell DISEASE- symptoms - Heterozygous form HbS + Hb A sickle cell TRAIT- usually no symptoms "carriers"
26
sickle cell clinical features
usually develop in childhood at age 4-6m - initial symptom is swelling at the digits - delayed growth and development - Increased susceptibility to infections - functional asplenia - aplastic crisis associated with Parvovirus B19 symptoms precipitated by hypoxic conditions - dehydration - high altitude - intense exercise
27
sickle cell clinical features
- chronic hemolysis * aplastic crisis: sudden decrease in HgB may be life threatening - vaso-occlusive ishemic tissue injury - PAIN CRISIS (most common feature) - osteonecrosis of femoral and humeral heads - ACUTE CHEST SYNDROME - CVA, MI - Splenic infarcts -> functional asplenia - skin ulcers - renal infarcts -> inability to concentrate urine -CHF, pulmonary HTN, dyspnea
28
sickle cell lab findings
- normocytic normochromic anmeia - increase in reticulocyte count - thrombocytosis may be present - HGB ELECTROPHORESIS reveals Hb S (best test to confirm sickle cell) - PERIPHERAL SMEAR: a few sickled RBCs nucleated RBCs, target cells, HOWELL-JOLLY BODIES, thrombocytosis
29
sickle cell disease treatment
- avoid precipitating factors - ANALGESICS, FLUIDS, and OXYGEN during pain crisis - RBC transfusions if needed - vaccination against encapsulated organisms - folate supplementation - HYDROXYUREA (chemo) to decrease incidence of painful crises (suppresses bone marrow function of all cell lines) - Bone marrow transplant*
30
what is autoimmune hemolytic anemia (AIHA)
caused by autoantibodies that adhere to the surface of RBCs and induce hemolysis by fixing complement and damaging the cell membrane -RBCs with antigen-antibody complex are phagocytized by macrophages and spherocytes are formed -> become smaller and are destroyed in the spleen
31
autoimmune hemolytic anemia differences between primary and secondary -deference between warm and cold
Primary: no underlying systemic disorder Secondary: identifiable underlying systemic illness IgM : cold agglutinins (stick together and lower than normal body temp) IgG: warm agglutinins at risk for VTE
32
AIHA causes/associations
- autoimmune or connective tissue diseases(SLE, RA) - hematologic malignancy (CLL) - infection (MYCOPLASMA, EBV, HIV) - immunodeficiency (prior solid organ or stem cell transplant) - prior blood transfusion - drugs
33
AIHI clinical features
- typical symptoms of (hemolytic) anemia (pallor, jaundice, splenomegaly) - fevers, fatigue, weakness, dyspnea - lymphadenopathy - hemoglobinuria - acrocyanosis- dark purple to gray discoloration of fingertips, toes, nose in exposure to cold
34
AIHI lab findings
-polychromasia spherocytosis and a nucleated RBC POSITIVE COOMBS TEST (DAT)
35
AIHI treatment
- depends on "warm" or "cold" disease and age - "cold" AIHA does not need to be treated in most children, usually mild and self-limited warm - CORTICOSTEROIDS ARE THE FIRST LINE - rituximab: antibody that targets B cell lymphocytes - splenectomy - immunosuppressants, IVIG Cold - AVOID COLD EXPOSURE - rituxumab - plasmapheresis if refractory
36
what is intravascular hemolysis
destruction of RBCs within the blood stream
37
what is fragmented syndrome
mechanical heart valve destroys RBCs into Schistocyte
38
what are hemolytic transfusion reactions
- blood transfusion reactions - hemolytic disease of the newborn HDN - coombs test can detect antibodies of the patient coating the transfused red cells Symptoms - FEVER - hemoglobinuria - severe hypotension - severe flank pain - pain at infusion site - chest tightness - DIC (oozing from IV site) - N/V/D
39
what is paroxysmal nocturnal hemoglobinuria
rare acquired stem cell mutation | -complemented mediated RBC lysis
40
Paroxysmal nocturnal hemoglobinuria clinical features
- hemolytic anemia - dark cola-colored urine at night/early AM, partial clearing during the day - venous thrombosis of large vessels - pancytopenia
41
Paroxysmal nocturnal hemoglobinuria diagnosis
- flow cytometry - osmotic fragility test - coombs negative -may progress to MDS/AML
42
paroxysmal nocturnal hemoglobinuria treatment
- monoclonal antibody against complement C5 - steroids - stem cell transplant
43
treatment of hemolysis
- identify and treat the underlying cause - corticosteroids can be helpful - splenectomy is frequently advised - folic acid supplementation recommended
44
what is aplastic anemia
an aquired abnormality of hematopoietic stem cells -may be total, or selective for RBCs, WBCs, or platelets - >50% of cases are "idiopathic" - 20% due to drug or chemical exposure (benzene, chloramphenicol, chemo) - 10% associated with viral illness (epstein-barr, cytomegalovirus, hepatitis) - ionizing radiation also causative
45
aplastic anemia clinical features
- PANCYTOPENIA is the hallmark - anemia (and reticulocytopenia) - leukopenia - thrombocytopenia - Bone marrow shows absence of precursors of these cells (normoblasts, granulocytes, and megakaryocytes) - clinical features due to above problems: weakness, infections, bleeding
46
aplastic anemia treatment
- identify cause and eliminate it - differentiate it from other serious illness that may require different treatment - hematology referral - transfusions as needed - bone marrow transplant preferred treatment - immunosuppressants if not BMT
47
normochromic, normocytic anemia
-with increased reticulocyte count prior or recent hemorrhage recent acute hemolysis ``` -with normal reticulocyte count: normal bone marrow: anemia of chronic disease hypothryroidism liver disease ``` With abnormal bone marrow: myelofibrosis, leukemia, myeloma, metastases, renal failure

Clin Med 1 (11 decks)

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