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Pharm > Anemia > Flashcards

Anemia Flashcards

1
Q

define anemia

A
  • male Hb < 13.5 g/dL
  • female Hb < 12 g/dL
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2
Q

what are clinical consequences of anemia

A
  • conjunctival pallor
  • atrophic glossitis
  • fatigue → lethary (depending on severity)
  • bounding pulses, palpitations, chest pain
  • high output congestive heart failure, MI (severe anemia)
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3
Q

what are the essential building blocks in heme production and RBC maturation (hematopoeisis)

Renal ___ provides cytokine signaling for RBC maturation and release from bone marrow

A

dietary iron, folate, B12

Renal EPO provides cytokine signaling for RBC maturation and release from bone marrow

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4
Q
  1. dietary iron is absorbed in the ____
A
  1. dietary iron is absorbed in the duodenum
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5
Q
  1. Fe 2+ may be stored in the ___ bound with apoferritin to produce the storage form ___
A
  1. Fe 2+ may be stored in the enterocyte bound with apoferritin to produce the storage form ferritin
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6
Q
  1. Fe 2+ released from basolateral enterocyte surface via ____
A
  1. Fe 2+ released from basolateral enterocyte surface via ferroportin 1
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7
Q
  1. Fe 2+ is oxidized to Fe 3+ by ___
A
  1. Fe 2+ is oxidized to Fe 3+ by ferroxidase
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8
Q
  1. Fe3+ is bound and transported in the blood via ____ to sites of erythropoiesis: ____, and to the ___ where it binds to apoferritin for storage
A
  1. Fe3+ is bound and transported in the blood via transferrin to sites of erythropoiesis: bone marrow, and to the liver where it binds to apoferritin for storage
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9
Q
  1. When ferritin is filled, hepatocytes produce ___ which feeds back on enteric iron absorption to ____ ferroportin 1 activity
A
  1. When ferritin is filled, hepatocytes produce hepcidin which feeds back on enteric iron absorption to downregulate ferroportin 1 activity
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10
Q

duodenal iron absorption: ___ mg/day

iron recycling in liver and spleen: ___ mg/day

A

duodenal iron absorption: 1 mg/day

iron recycling in liver and spleen: 30 mg/day

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11
Q

in iron deficiency, what lab findings do you see?

transferrin saturation ?
ferritin ?
TIBC ?

A
  • *decreased** transferrin saturation
  • *decereased** ferritin
  • *increased** TIBC
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12
Q

___ route is preferred in iron therapy

A

oral route is preferred in iron therapy

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13
Q

__ iron is best absorbed

A

ferrous (Fe2+) iron is best absorbed

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14
Q

list the ferrous iron oral drugs and what is co-administered for optimal absorption?

A
  • ferrous sulfate
  • ferrous gluconate
  • ferrous fumarate
  • ascorbic acid for optimal absorption
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15
Q

when do you give parenteral iron therapy?

A

chronic renal failure patients (high iron requirement)

hemodialysis patients (in combo with EPO)

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16
Q

list the parenteral iron formulations

A
  • iron dextran - highest risk for type 1 HSN
  • sodium ferric gluconate complex
  • iron sucrose
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17
Q

list adverse affects of iron therapy

A
  • black stool
  • GI
    • nausea
    • epigastric discomfort
    • abdominal cramps
    • constipation
    • diarrhea
18
Q

what is the presentation of acute iron toxicity?

A
  • history of iron ingestion by children
  • direct GI irritation
    • acue vomiting
    • diarrhea
    • abdominal pain
    • mucosal ulceration and bleeding
19
Q

describe the pathogenesis for acute iron toxicity

A
  • free iron disrupts critical cellular processes
    • metabolic acidosis
    • widespread organ toxicity → shock, coma, death
  • abdominal radiographs showing radio-opaque pills in stomach
20
Q

how do you treat acute iron toxicity?

A
  • activated charcoal is NOT effective (does not bind to iron)
  • supportive care
  • iron chelators:
    • Deferoxamine
    • Deferasirox
21
Q

contrast deferoxamine and deferasirox

A
  • deferoxamine
    • given IV to bind system iron
    • promotes iron excretion (urine/feces)
    • moderate & severe iron toxicity
  • deferasirox
    • oral
    • only effective at reducing iron absorption if given within 1 hour of ingestion
    • used for chronic iron toxicitiy → outpatient iron chelation in transfusion dependent individuals
22
Q

what can cause chronic iron toxicity?

A
  • hemochromatosis
    • cardiomyopathy
    • bronze diabetes
    • cirrhosis
  • patients requiring frequent blood transfusions (thalassemia major)
23
Q

desribe B12 absorption

A
  • consumed in animal products
  • salivary R binders bind to free B12
  • pancreatic enzymes break up the complex and binds of IF from parietal cells → duodenum
  • IF-cobalamin complex absorbed in terminal ileum
  • transported bound to glycoproteins as transcobalamin I, II, III
24
Q

The main storage site of B12 is in the ____ and takes ____ to develop B12 deficiency

A

The main storage site of B12 is in the liver and takes 5 years to develop B12 deficiency

25
Q

list causes of B12 deficiency

A
  • insufficient ingestion (strict vegans)
  • defects in cobalamin absorption
    • autoimmune disease: prenicious anemia
    • surgery: gastrectomy, ileal resection
    • small bowel disease: crohn’s, celiac, fish tapeworm infection (diphyllobothrium latum)
  • Drugs
26
Q

what drugs cause B12 deficiency?

A
  • metformin, neomycin: alter gut flora
  • nitrous oxide anethesia: converts cob(I)alamin to inactive form cob(III)alamin
  • proton pump inhibitors, histamine 2 receptor antagonists: increase gastric pH
27
Q

describe the clinical presentaiton of vitamin B12 deficiency

A
  • anemia
  • neurological symptoms
    • parethesias
    • subacute combined degeneration of spinal cord d/t abnormal myelination synthesis
    • prolonged deficiency = irreversible nerve damage
  • skeletal changes
    • suppressed osteoblast activity → osteoporosis
28
Q

what are the lab studies in B12 deficiency?

A
  • megaloblastic macrocytic anemia
  • leukopenia and/or thrombocytopenia
  • decreased B12
  • +/- antibodies agaist IF
  • increased homocysteine
  • increased methylmalonate
  • increased methylmalonyl-CoA
29
Q

explain B12 deficiency therapy and its adverse effects

A
  • must be parenteral and continued for the duration of malabsorption
  • hydroxycobalamin
    • ​preferred highly-protein bound form → stays in circulation longer
  • cyanocobalamin
  • no adverse effects!
30
Q

what is the most common nutrient deficiency in USA?

A

Folate deficiency

31
Q

describe folate absorption

A
  1. polyglutamylated dietary folate cleaved to monoglutamate via brush border enzymes in the jejunum
  2. enteres plasma via active and passive mechanisms
  3. in peripheral tissue: polyglutamylated again so it cannot diffuse into the plasma
  4. healthy individuals take 4-5 months for folate depletion (small hepatic store)
32
Q

list risk factors for folate deficiency

A
  • advanced age
  • pregnancy
  • chronic hemolytic anemias eg. sickle cell anemia
  • alcohol abuse
  • drugs
33
Q

what drugs causes folate deficiency?

A
  • inhibitors of DHF:
    • trimethoprim
    • pyrimethamine
    • methotrexate
  • phenytoin
34
Q

describe the presentation of folate deficiency

A
  • anemia
  • no neurological sympytoms
  • fetal neural tube defects in 1st trimester of pregnany
35
Q

describe folate deficient lab study

A
  • megaloblastic macrocytic anemia
  • decreased folate levels
  • increased homocysteine
  • normal methylmalonic acid
36
Q

describe folate therapy

A
  • folic acid given orally for 1-4 months or until complete hematological recovery occurs
  • prophylactic supplements should be give for:
    • pregnant
    • alcohol dependent
    • hemolytic anemia
    • liver disease
    • exfoliative skin disease
    • renal dialysis
37
Q

list/describe erythrocytic growth factors

A
  • erythropoeitin & darbepoetin
  • stimulates JAK/STAT receptors
  • Given parenterally in:
    • chronic renal failure
    • bone marrow suppression
  • AE: hypertension, thrombosis
38
Q

list/describe myeloid growth factors

A
  • Filgrastim (G-CSF)
  • Sargramostin (GM-CSF)
  • stimulates JAK/STAT receptors
  • increases production/function of neutrophils
  • Sargramostin stimulates all myeloid pregenitor cells
  • given parenterally in:
    • ​cancer chemotherapy induced neutropenia
    • bone marrow suppresion
  • AE: bone pain, filgrastim = better tolerated
39
Q

Describe interleukin 11

A
  • myeloid growth factor
  • acts via cell surface cytokine receptor
  • stimulates growth of primitive megakaryocuytic progenitors
  • increase platelets and neutrophils
  • reduces need for platelet transfusions in chemotherapy recipients with prior episodes of thrombocytopenia
40
Q

describe hydroxyurea

A
  • reduces vascular occlusion in SCD
  • increases HbF (reduces sickling)
  • decreases expansion of neutrophil adhesion molecules
  • increases endothelial production of NO

Pharm (6 decks)

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