Do I Make You Sweat(man)? Flashcards

1
Q

what are the three irons administered for Fe deficiency?

A

ferrous sulfate
ferrous gluconate
ferrous fumerate

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2
Q

what is the difference between ferrous and ferric iron?

A

ferrous is “just the 2+ of us”

ferric is 3+

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3
Q

how much Fe is absorbed with oral supplementation?

A

25%

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4
Q

how much Fe can be incorportated in Hgb per day?

A

50-100mg

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5
Q

if you were wanting to correct a Fe def ASAP, how much would you admin? why?

A

200-400

absorb 25% :: will max out daily utilization at 50-100

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6
Q

after you correct the deficiency, how much longer do you admin Fe?

A

3-6 mo to replete stores

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7
Q

what are the related toxicities related to oral iron?

A

GI probs: nausea, epigastic discomfort, abdominal cramps, constipation, diarrhea

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8
Q

what is the most common cause of chronic anemia?

A

iron deficiency

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9
Q

what are the symptoms of anemia?

A
pallor
fatigue
dizziness 
exertional dyspnea
generalized symptoms of tissue hypoxia
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10
Q

what is a special adaption to chronic anemia?

A

CV adaptations

tachycardia, increased output, vasodilation

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11
Q

what is an underlying disease to be aware of for iron-def pts?

A

CV issues - Fe def can exacerbate

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12
Q

where is the Fe used for hematopoiesis from?

A

from senescent or damaged erythrocytes that are recycles

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13
Q

where is the most common place of blood loss for men and p-m women?

A

GI

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14
Q

adjustments you can make to try to avoid AE of oral iron

A
  • dose-related :: lower daily dose
  • take with or after meals
  • try a different iron salt
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15
Q

what is a special side effect of oral iron you need to be aware of?

A

turns stools black :: could obscure a GI bleed **

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16
Q

what type of iron do you give orally? parenterally?

A

oral - ferrous

parenteral - ferric

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17
Q

parenteral iron is indicated in what pts?

A
  • cannot tolerate oral
  • extensive chronic anemia
  • renal disease 2* Epo admin, dialysis
  • proximal bowel/duodenum involvement
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18
Q

what is absorbed in the duodenum? jejunum? ileum?

A

duodenum - Fe
jejunum - folate
ileum - B12

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19
Q

what is the important thing about parenteral iron? why?

A

serious dose-dependent toxicity

bypasses body’s innate regulation

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20
Q

toxicity symptoms for parenteral iron?

A
  • hypersensitivity Rx: headache, light head, arthalgias, N+V, back pain, flushing, urticaria, bronchospasm
  • (!) : possible anaphylaxis and death **
  • give small test dose
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21
Q

what is the name of the iron that you admin parenterally?

A

Fe Dextran

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22
Q

what values can you use to estimate iron stores?

A
  • ferritin
  • transferrin
  • % sat’n
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23
Q

what is the % sat’n?

A

(serum Fe)/ (TIBC)

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24
Q

symptoms of acute Fe toxcitiy

A

shock, lethargy, dyspnea,
bloody diarrhea
vomiting, abdominal pain
initial improvement followed by severe metabolic acidosis –> coma –> death!**

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25
Q

which iron-overload Tx is given IV? orally?

A

IV - Deferoxamine

oral - Defasirox

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26
Q

what is Deferoxamine? how does it affect other metals? how is it excreted?

A
  • iron chelating for iron-overload
  • doesn’t chelate impt trace metals
  • bile, urine (red!)
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27
Q

side effects of Deferoxamine

A
  • tachycardia, hypotension, shock

- could add to CV collapse from iron-toxicity**

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28
Q

what are types of chronic iron toxicity?

A

Hemochromatosis

Thalassemmia Major 2* transfusions

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29
Q

what is Defasirox? how can it be admined?

A
  • for chronic iron overload (e.g., due to multiple blood transfusions)
  • also for iron ingestion overload/toxicity
    :: for chronic and acute
  • orally with OJ
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30
Q

why OJ with oral Fe?

A

vit C/ascorbate helps Fe absorb better

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31
Q

some side effects of Defasirox

A
  • diarrhea, nausea, abdominal pain, headache
  • pyrexia/fever, cough
  • increased serum creatinine and liver enzyme levels **
  • auditory + visual disturbances **
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32
Q

what is the best Tx for chronic iron overload without anemia?

A

bleeding

1 u/week

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33
Q

what is another name for vit B12?

A

cobalamin

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34
Q

give me some physical symptoms of B12 def

A

GI

neurologic abnormalities

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35
Q

why do you get the crazies with B12 def?

A

because there is a buildup of proprionlyl CoA due to the buildup of me-malonic acid/me-CoA

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36
Q

what population is B12 def most likely in?

A

vegans

olds

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37
Q

give me some hematologic symptoms of B12 def

A
  • megaloblastic erythroid cells
  • macrocytic (in ALL cells, not just RBCs)
  • pancytopenia: leukopenia and/or
  • thrombocytopenia
  • hypercellular bone marrow
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38
Q

what are causes of B12 def if not from dietary def? what is the general mechanism?

A
  • Pernicious Anemia
  • involvement of distal ileum

gen mechanism: malabsorbtion

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39
Q

rare causes of B12 def

A

bacterial overgrowth
chronic pancreatitis
thyroid dis
children w/ congenital IF def or IFR

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40
Q

what is parenteral Tx for B12 def?

A

shots shots shots shot shot shotssss

errryyybody

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41
Q

what are the vitamin versions of B12? which one is preferred? why?

A

Cyanocobalamin
Hydroxycobalamin

Hydroxy > Cyano bc more protein bound :: remains in circulation longer

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42
Q

what form of folic acid do you need for biochemical reactions?

A

reduced

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43
Q

what is a more common def, B12 or folate?

A

folate

44
Q

how long does it take to develop a folate def? a B12 def?

A

folate: 3-4 mo
B12: 2-4 years

45
Q

what pop are at risk for folic acid def?

A
alcoholics
liver disease
pregnant women
hemolytic anemia pts
dialysis pts
certain skin diseases
46
Q

is oral absorption of FA high or low?

A

high

even in a pt with a malabs syndrome

47
Q

what drugs cause a deficiency in FA?

A

Methotrexate
Trimethoprim (antimicrobial)
Pyrimethamine (antimalarial)
Phenytoin (antiepileptic)

48
Q

how does Phenytoin cause FA def?

A

inhibiting intestinal uptake of FA

49
Q

tell me about Leucovorin.

A
  • Leucovorin is the knight that saves FA Princess from the evil folate antagonists
  • he is also a do-gooder and modulates 5-FU/fluorouracil in his fight against the cancers
  • he is a reduced folate
50
Q

why are you more likely to get a FA def from Trimethoprim or Pyrimethamine rather than Phenytoin?

A

bc they have a higher affinty for the bacterial and malarial FA

51
Q

tell me about folate and depression. why did they think that it might work to make the depressed happy puppies of sunshine?

A
  • FA (in a different form) modulates formation of NT like serotonin, norepi, dopa
  • study says: might work
52
Q

the best enzyme, MTHFR, takes what to what? what pathway does this play a role in?

A

FA, DHF to Levomofolate

related to monoamine neurotransmitter synthesis

53
Q

what is the biologically active form of folate found in the circulation?

A

Levomofolate

aka 6-5-MeTHF, L-MeFolate

54
Q

what makes Levomofolate so special? how does it do this special thing?

A

it can cross the BBB

receptor-mediated endocytosis

55
Q

what is the name of the hematopoietic growth factor med? what is it’s mechanism?

A

rHuEPO aka Epo alfa

agonist of Epo receptors expressed by red cell progenitors

56
Q

what does a PEG prefix mean?

A

PEG = polyethylene glycol

the original drug has had PEG added to it

57
Q

what does adding PEG to a drug do?

A
  1. extend the PK

2. reduce the need for so frequent re-dosing

58
Q

what does Epo alfa do?

A
  • stimulates erythroid prolif, diff

- release of retics from bone marrow

59
Q

what is Darbopoietin alfa?

A

long acting form
weekly vs. every few days

glycosylated

60
Q

what is Methoxy polyethylene glycol also called?

A

Epo beta

long acting form
1-2x month

61
Q

what is the toxcicity that comes with Epo alfa?

A

HTN
thrombotic complications
pure red cell aplasia (very rare) **

62
Q

why the special concern with managing Hgb levels with Epo?

A

bc there are CV risks with >12 g/dL

63
Q

what is Epo alfa used to treat?

A
  • anemia (no shit)
  • renal failure assoc anemia
  • HIV
  • infection
  • Cx
  • prematurity
64
Q

how is Epo alfa used in the OR? what are the risks that come with this?

A

can be used instead of a blood transfusion

increased DVT risk :: DVT prophylaxis

65
Q

what special receptor family are the hematopoietic growth factors involved with?

A

JAK/STAT cytokine receptor

posphorylation, Tx factors to regulate cell function

66
Q

what induces production of endogenous epo?

A

hypoxia

67
Q

epo serum levels for helathy, mod severeanemia, and severe anemia

A

normal: <20 IU/L
moderate: 100-500
severe anemia: 1000s

68
Q

what are epo levels in renal disease? on primary bone disorders? nutritional anemias? secondary anemias?

A

low

rest high

69
Q

will a person with high or low epo be responsive to exogenous Epo?

A

low :: renal disease pts will respond

70
Q

what are the two BBW for Epo?

A

chronic kidney disease **

Cx **

71
Q

why is chronic kidney disease a BBW for Epo?

A
  • greater risk of death, stroke, serious CV AE **

- no known dose or dosing strategy to reduce these risks **

72
Q

why is Cx a BBW for Epo?

A
  • shortened overall survival and/or **

- increased risk of tumor progression **

73
Q

when should an ESA be used?

A
  • for anemia due to myelosupressive Tx **

- DON’T use when pt is curable **

74
Q

which Epo is better to use, alfa or beta?

A

alfa

beta had more deaths assoc with it when used for Tx of anemia from chemo **

75
Q

what does Lance Armstrong use?

A

Epo :: why it’s banned

76
Q

what is Zidovudine?

A
  • Tx for HIV pts
  • can cause anemia
  • Epo can offset this anemia
77
Q

Epo can be used to treat what two specialized populations?

A

HIV anemics and preemies

78
Q

what are the myeloid growth factors?

A

G-CSF/filgrastin
Pegfilgrastin
GM-CSF/sargramostim

79
Q

what are the Fe-def drugs?

A

ferrous sulfate
ferrous gluconate
ferrous fumerate
Iron Dextran

80
Q

what are the FA def drugs?

A

Folic Acid
Leucovorin
Levomofolate

81
Q

What are the hematopoietic growth factors?

A

Epo alfa
Darbepoetin
Me-PEG Epo beta

82
Q

what are the megakaryocyte growth factors?

A

Oprelvekin (IL-11)

Romiplostin

83
Q

what does G-CSF do?

A
  • prolif, diff of neutrophil progenitors
  • activates neutrophil phagocytotic activity
  • extends survival of neutrophils
  • mobilizes hematopoietic stem cells, i.e., inc their concentration in blood
84
Q

what is G-CSF used for?

A
  • neutropenias assoc myelodysplasia
  • neutropenias assoc aplastic anemia
  • chemo pts - secondary prevention of neutropenia
  • stem cell transplant - mobilizes perpheral blood cells
85
Q

what receptor family are myeloid growth factors in?

A

JAK/STAT

86
Q

G-CSF v. GM-CSF

A

G-CSF: prolif, diff of progenitors already committed to neutrophil lineage
GM-CSF: early and late granulocytic progenitor cells

[think: GM-CSF acts earlier in the family tree]

87
Q

which myeloid GF allows for use of peripheral blood stem cells in stem cell transplants? why is this beneficial?

A

G-CSF

can use PBSCs rather than bone marrow stem cells

88
Q

what is GM-CSF used for?

A
  • prolif, diff of early AND late granulocytic progenitor cells
  • erythrocyte and megalaryocyte progenitors
  • function of mature neutrophils
  • stimulate T cell prolif with IL-2
89
Q

which cytokine does GM-CSF work with? what does it do?

A

IL-2

stimulate T cell prolif

90
Q

which mobilizes peripheral stem cells better, G-CSF or GM-CSF?

A

G-CSF

91
Q

even though G-CSF accelerates the rate of nutro recovery, what can it NOT do?

A

increase pt survival

92
Q

what is the benefit to Pegfilfrastim?

A
  • admin’d less frequently

- shorten the window of severe neutropenia > G-CSF

93
Q

what happens first with admin of G-CSF, recruitment of mature neuto or new neutro production?

A

recruitment of the already exsisting

94
Q

which myeloid GF are used more often? why?

A

G-CSF and Pegfilgastim

better tolerated

95
Q

what is a side effect of discontinuing myeloid GF?

A

bone pain

96
Q

toxic/side effects from myeloid GF?

A
  • capillary leak syndrome (characterized by) **
  • peripheral edema (and)
  • pleural or pericardial effusion **
  • splenic rupture, rare ** (in PBSC)
  • rare Ax Rx
  • more side effects with GM-CSF
  • fever, malaise, arthalgias, myalgias
97
Q

what is a rare, but serious side effect of PBSC?

A

splenic rupture

well, shit.

98
Q

what is Oprelvekin?

A

rh-IL-11

99
Q

what does Oprelvekin do?

A
  • stim growth of megakaryocyte prgenitors
  • stim growth of lymphoid, myeloid cells
  • inc number of circulating platelets and neutrophils
100
Q

what is Romiplostin?

A
  • megakaryocyte GF peptibody
  • 2 identical, single chain IgG1
  • Fc of IgG1 covalently linked two identical copies of a peptide that stimulates thrombopoietin/TPO receptors
101
Q

what is Romiplostin used to treat?

A

TPP

102
Q

what family of receptors is Oprelvekin in?

A

a family that can all interact with gp130

103
Q

what is a point of comparison between Oprelvekin and G-CSF?

A

G-CSF increases survival of neutrophils, whereas Oprelvekin-stimulated platelets have normal life expectancies

104
Q

what is Oprelvekin used to treat?

A

thrombocytopenia, a secondary prevention in pts getting chemo for nonmyeloid Cx

105
Q

what are some toxic effects of Oprelvekin?

A
  • CV
  • anemia 2* hemodilution **
  • dyspnea 2* fluid accumulation in the lungs **
  • transient atrial arrhythmias
  • hypokalemia **
106
Q

what is the benefit of the FcR in Romiplostin?

A

extends half life :: remains active in the circulation longer than endogenous tpo