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Clin Med 1 > Anemia 2 > Flashcards

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
Q

what is sickle cell

A
  • 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
Q

sickle cell clinical features

A

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
Q

sickle cell clinical features

A
  • 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
Q

sickle cell lab findings

A
  • 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
Q

sickle cell disease treatment

A
  • 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
Q

what is autoimmune hemolytic anemia (AIHA)

A

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
Q

autoimmune hemolytic anemia differences between primary and secondary
-deference between warm and cold

A

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
Q

AIHA causes/associations

A
  • 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
Q

AIHI clinical features

A
  • 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
Q

AIHI lab findings

A

-polychromasia spherocytosis and a nucleated RBC

POSITIVE COOMBS TEST (DAT)

35
Q

AIHI treatment

A
  • 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
Q

what is intravascular hemolysis

A

destruction of RBCs within the blood stream

37
Q

what is fragmented syndrome

A

mechanical heart valve destroys RBCs into Schistocyte

38
Q

what are hemolytic transfusion reactions

A
  • 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
Q

what is paroxysmal nocturnal hemoglobinuria

A

rare acquired stem cell mutation

-complemented mediated RBC lysis

40
Q

Paroxysmal nocturnal hemoglobinuria clinical features

A
  • hemolytic anemia
  • dark cola-colored urine at night/early AM, partial clearing during the day
  • venous thrombosis of large vessels
  • pancytopenia
41
Q

Paroxysmal nocturnal hemoglobinuria diagnosis

A
  • flow cytometry
  • osmotic fragility test
  • coombs negative

-may progress to MDS/AML

42
Q

paroxysmal nocturnal hemoglobinuria treatment

A
  • monoclonal antibody against complement C5
  • steroids
  • stem cell transplant
43
Q

treatment of hemolysis

A
  • identify and treat the underlying cause
  • corticosteroids can be helpful
  • splenectomy is frequently advised
  • folic acid supplementation recommended
44
Q

what is aplastic anemia

A

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
Q

aplastic anemia clinical features

A
  • 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
Q

aplastic anemia treatment

A
  • 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
Q

normochromic, normocytic anemia

A

-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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