ch 47 Flashcards

1
Q

Most deficiency anemias result from deficiency of what 3 things?

A

Iron, vitamin B12 or folic acid

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2
Q

What is the earliest stage of RBC development and what are they missing?

A

proerythroblasts and they lack hemoglobin

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3
Q

what is the second stage of RBC development and what have they gained?

A

erythroblasts, they have gained hemoglobin

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4
Q

Where do erythroblasts and proerythroblasts reside

A

Bone marrow

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5
Q

What is the third stage of RBC development and where do they go

A

reticulocytes - enter systemic circulation (immature erythrocytes)

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6
Q

At full maturity what are the RBCs known as

A

erythrocytes

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7
Q

what is the most common nutritional deficiency

A

iron

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8
Q

what is the max absorptive capacity of iron

A

3-4mg/day

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9
Q

what enhances absorption of iron

A

Vit C

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10
Q

What reduces absorption of iron

A

food

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11
Q

after uptake of iron, what are the 2 pathways it can undergo?

A

Storage within mucosal cells in the form of ferritin (iron plus a protein used to store iron)

Binding to transferrin (the iron transport protein) for distribution throughout the body

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12
Q

What are the 4 potential fates for transferrin bound iron

A

1) taken up by cells of the bone marrow for incorporation into hemoglobin - most
2) taken up by the liver and other tissues for storage as ferritin
3) taken up by muscle for production of myoglobin
4) taken up by all other tissues for production of iron-containing enzymes

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13
Q

explain the recycling of hgb

A

After 120 days of useful life, RBC s are catabolized. iron is released by this process and reenters the plasma bound to transferrin and the cycle starts over

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14
Q

how is iron excreted

A

excretion is minimal (if no iron was replaced the body stores would only drop 10% per year)

Most through bowel, some through urine and sweat

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15
Q

regulation of iron

A

through intestinal absorption

as body stores rise, uptake of iron declines
as body stores become depleted, uptake increases

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16
Q

Requirements for iron are determined by what?

A

rate of erythrocyte production

when RBC production is low, iron needs are low too
when high, iron needs are high

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17
Q

daily iron need of adult men

A

8mg dietary iron daily

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18
Q

daily iron need of adult women

A

15-18 mg per day to replace iron lost through menstruation

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19
Q

daily iron need for pregnant women and 2-3 months after pregnancy

A

need iron supplement of about 27mg per day bc diet will not be enough

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20
Q

what are the most common causes of increased iron demands?

A

1) pregnancy
2) blood volume expansion during infancy and early childhood
3) Chronic blood loss, usually GI or uterine origin

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21
Q

In the absence of iron for hemoglobin synthesis red blood cells become _____ and ____

A

microcytic and hypochromic

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22
Q

symptoms of reduced oxygen carrying capacity of blood

A

listlessness
fatigue
pallor of skin
pallor of mucous membranes

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23
Q

symptoms of severe tissue oxygen comprimise

A

tachycardia
dyspnea
angina

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24
Q

iron deficiency anemia is a ______anemia

A

microcytic

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25
Q

Vitamin B deficiency and folate deficiency anemias are considered ______ anemia

A

Megaloblastic

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26
Q

What are common causes of anemia

A
poor diet
chronic blood loss (menorrhagia, colon polyp, hemorrhoids)
celiac disease
lack of intrinsic factor
enteritis
low dietary intake
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27
Q

what two oral preps most often used for iron supplementation

A
ferrous salts (ferrous sulfate)
carbonyl iron
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28
Q

what is the treatment of choice for iron deficiency anemia or to prevent this during increased needs such as pregnancy or chronic blood loss

A

Ferrous sulfate (also more cost effective)

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29
Q

adverse effects of ferrous sulfate

A
nausea
heartburn
bloating
constipation
diarrhea

most intense during initial therapy and become less disturbing with continued use

may turn stools dark green or black - harmless and not a sign of Gi bleeding

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30
Q

Patients with what disorders should not take oral iron supplements?

A

Peptic ulcers
Regional enteritis
ulcerative colitis

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31
Q

what color can ferrous sulfate make the stool

A

dark green or black and is harmless - do not interpret this as a sign of gi bleeding

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32
Q

How do you prevent tooth staining while taking an liquid iron supplement

A

diluting liquid with juice or water
administering the iron through a straw or with a dropper
Rinsing mouth out after administration

33
Q

in young children, what is the leading cause of poisoning fatalities?

A

Iron containing products

rare in adults

34
Q

what is the lethal dose of iron in children

A

2 to 10g

35
Q

antacids do what to the absorption of iron

A

reduce

36
Q

coadministration of iron with tetracyclines _____ the absorption of both

A

decrease

37
Q

iron and ascorbic acid (vit c)

A

Vit c promotes absorption but combining the 2 offers no advantage over a simple increase in iron dose

38
Q

Carbonyl iron and safety

A

higher margin of safety - requires a much higher dose to cause serious harm

good bioavailability
therapeutic efficacy equal to ferrous salts

39
Q

what are the timelines for improvement with therapy

A

reticulocytes will increase within 4-7 days
1 week you will see increases in hgb and hct
1 month hemoglobin levels will rise by at least 2g/dl

40
Q

if levels are not improving, what should the patient be evaluated for?

A

compliance
continued bleeding
inflammatory disease
malabsorption of oral iron

41
Q

combining iron therapies

A

should be avoided. They should not be receiving iron in more than one route at one time.

42
Q

what other supplements should be avoided during iron therapy

A

avoid combo with vitamin B12 or folic acid

43
Q

members of the vitamin B12 family are known as

A

cobalamins

44
Q

How does vit B12 influence cell growth and division

A

by permitting the utilization of folic acid

45
Q

efficient absorbption of vit b12 requires

A

intrinsic factor

46
Q

in most cases vit b 12 def is result of

A

Impaired absorption

47
Q

potential causes of impaired absorption

A

regional enteritis
celiac diseae
developed antibodies against vit 12-intrinsic factor complex -
bariatric surgery
someone who takes alot of acid reducing agent (need stomach acid to extract B12 from food

48
Q

impaired absorption of b12 occurs secondary to _____

this is called _______________

A

lack of intrinsic factor which is called pernicious anemia

49
Q

what do you see in bone marrow in blood for megaloblastic or macrocytic anemia

A

large number of megaloblasts (oversized erythroblasts) appear in the bone marrow and macrocytes (oversized erythrocytes) appear in the blood

50
Q

what is the principal cause of mortality from b12 def

A

severe anemia causes peripheral and cerebral hypoxia leading to heart failure and dysrhythmias causing death

51
Q

hematologic effects of vit b12 deficiency can be reversed by

A

large doses of folic acid (will not improve the neurological pic)

52
Q

Neurologically what happens in b12 deficiency

A

demyelination of neurons, primarily in spinal cord and brain

53
Q

symptoms of demylenination

A

paresthesias of hands and feet
reduction in deep tendon reflexes
late - loss of memory, mood changes, hallucinations, psychosis
if prolonged this can be permanent

54
Q

in addition to disrupting production of erythrocytes, lack of b12 also prevents

A

the bone marrow from making leukocytes (wbc) and thrombocytes (platelets) which can lead to infection and spontaneous bleeding

55
Q

for a pt with b12 deficiency exhibiting severe neuro effects what should be given?

A

parenteral cyanocobalamin

56
Q

primary manifestations of moderate B12 deficiency are

A

megaloblasts in the bone marrow and macrocytes in peripheral blood - can be managed with vit B12 alone

57
Q

what is the recommended treatment for severe B12 deficiency which disrupts all blood cells can lead to hypoxia, cerebrovascular insufficiency and heart failure

A

1) IM injection of Vitamin B12 and folic acid (folic acid accelerates recovery of hematologic deficits)
2) administration of 2-3 units of packed RBCs (to correct anemia quickly)
3) transfusion of platelets
4) therapy with abx if infection has developed

58
Q

for patients who lack intrinsic factor or suffer from some other permanent cause of vit b12 malabsorbption, lifelong treatment is required. What does therapy and monitoring look like

A

Monthly IM or SC injections of cyanocobalamin (B12) or
large daily oral doses or weekly intranasal doss

plasma levels of vit b12 drawn every 3-6 months with blood samples examined for return of macrocytes and blood counts performed

59
Q

hazard of folic acid in b12 deficiency

A

used to reverse hematologic affects but can mask b12 deficiency and neurological damage can continue to progress. take extra care to monitor B12 dosage when also using folic acid

60
Q

A patient presents with megaloblastic anemia, what type of deficiency could this be?

A

Folic acid
Vitamin B12
Both

61
Q

How does folic acid take the place of Vitamin B12 for DNA synthesis?

A

When large amounts of folate are ingested, some can be activated through an alternative pathway that does not employ vit B12 which is why a large dose can fix hematologic problems

62
Q

what are the 2 principal causes of folic acid deficiency

A
poor diet (esp in alcoholics)
malabsorption secondary to intestinal disease

can also be from increase in demand (pregnancy, hemodialysis patients

63
Q

what is the most common cause of folate deficiency

A

alcohol use disorder (reversible)

64
Q

what is SPRUE

A

an intestinal malabsorption syndrome that decreases folic acid uptake.

65
Q

How can Folate deficiency from Sprue be corrected

A

large doses of folic acid orally

66
Q

folate deficiency is _____ to vit b12 deficiency with the exception of ____

A

identical

it does not injure the nervous system

67
Q

_____ deficiency very early in pregnancy can cause neural tube defects such as spina bifida

A

folic acid

68
Q

the US preventative services task force now recommends that all women who may become pregnant consume ________________

A

400 to 800ug of supplemental folic acid each day in addition to the folate they get from food

69
Q

How should treatment of folic acid deficiency be initiated?

A

IM injection of folic acid and vitamin b12
After the initial injection, treatment should continue with folic acid alone
1000-2000 ug/day for 1-2 weeks
maintenance of 400ug/day may be required

70
Q

causes of iron deficiency due to reduced iron uptake

A

gastrectomy

SPRUE - disease of tropical regions is characterized by fatty diarrhea and malabsorption of nutrients

71
Q

GI blood loss could indicate

A

Peptic ulcer disease

GI cancer

72
Q

four ferrous iron salts

A

ferrous sulfate
ferrous gluconate
ferrous fumarate
ferrous aspartate

73
Q

potential causes of iron deficiency

A

pregnancy
bleeding
inadequate diet
impaired intestinal absorption

74
Q

the enterohepatic recirculation helps salvage up to ____ug of folate per day

A

200

75
Q

why are pt with alcohol use disorder at highest risk for folate deficiency

A

insufficient folic acid in diet

derangement of enterohepatic recirculation secondary to alcohol induced injury to the liver

76
Q

can folate deficiency be reversed in pt with alcohol use disorder

A

yes, with improved diet and reduced alcohol consumption, alcohol related folate deficiency will often reverse

77
Q

how do you treat folate deficiency in SPRUE

A

large doses of folic acid orally

78
Q

Plasma iron > 500, what should you do

A

toxic level, give parenteral deferoxamine

79
Q

What type of B12 deficiency is when you add folic acid

A

Severe