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PHAR 253 Final > Anemia > Flashcards

Anemia Flashcards

1
Q

What is anemia? What does it result in?

A

Decrease in the number of red blood cells or less than normal quantity of hemoglobin (Hgb) in the blood

Results in decreased oxygen carrying capacity in the blood

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2
Q

Anemia is…..

A

An objective sign of a disease

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3
Q

Etyiology of Anemia

A

Several etiologies

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4
Q

What dictates treatment of anemia?

A

Diagnosis is important to dictate tx

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5
Q

Where are RBC’s formed?

A

Bone Marrow

Termed erythropoiesis
Adults: spine, ribs, sternum, clavicle, pelvic crest, ends of long bones

Children: most bone marrow space

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6
Q

What do RBC contain? What makes it up?

A

RBCs contain hemoglobin:
–> protein component (2 alpha/2 beta chains)
–> heme (porphyrin ring + iron)

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7
Q

Is adult hemoglobin the same as a babies?

A

Two alpha and two gamma chains

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8
Q

Describe the process of Erythropoiesis

A
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9
Q

How long is the process of erthyropoiesis?

A

One week long (7 days)

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10
Q

What guides the process of erthropoiesis?

A

Works on a feedback loop

↓ tissue oxygen concentration signals the kidneys to ↑ production and release of EPO

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11
Q

What is the function of EPO?

A

stimulates stem cells to differentiate

↑ release of reticulocytes from bone marrow

induces Hb formation

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12
Q

What is the RBC turnover? Where does this occur?

A

120 Days

Mainly the spleen, some broken down by the bone marrow

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13
Q

Describe the normal cycle of erythropoiesis and turnover

A

Normally, this system is in balance

EPO matching new erythrocyte production to the natural rate of loss of RBCs

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14
Q

Anemia is a _______ of what?

A

A symptom of many pathological conditions

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15
Q

Anemia is associated with: (What may cause anemia?)

A

Nutritional deficiencies

Acute or chronic diseases

Drug induced

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16
Q

How can anemia be classified?

A

Pathophysiology or by morphology

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17
Q

What are the 3 main pathophysiological causes of anemia?

A

1) BLOOD LOSS
Trauma, ulcer, hemorrhoids etc. e.g. ASA

2) INADEQUATE RBC PRODUCTION
–> Nutritional deficiency: vitamin B12, folic acid iron
–> Erythroblast deficiency: bone marrow failure (aplastic anemia, irradiation, chemotherapy) or bone marrow infiltration (tumors, cancers)
–> Endocrine deficiencies
–> Chronic disease: ex renal, liver, infection

3) EXCESSIVE RBC DESTRUCTION
Autoimmune, drug, infection

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18
Q

How can anemia be classified by morphology?

A

Size
Microcytic
Normocytic
Macrocytic (to big)
–> megaloblastic
–> non-megaloblastic

Colour
Hypochromic (pale)
Normochromic
Hyperchromic (darker than normal)

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19
Q

How is the size of an RBC determined?

A

Size is reflected by the mean corpuscular volume (MCV)

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20
Q

Describe the specific sizes of RBC?

A

Microcytic: <80 fL (“small”)
Normocytic: 80-100 fL (“normal”)
Macrocytic: >100 fL (“big”)

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21
Q

How is the colour of an RBC determined?

A

Colour is reflected by the mean corpuscular Hb concentration (MCHC)

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22
Q

Describe the specific colours of RBC’s?

A

Hypochromic: pale
Normochromic: normally coloured
Hyperchromic: darker

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23
Q

What are the reasons why an anemia may be microcytic?

A

primarily a result of Hb synthesis failure or Hb insufficiency

can be due to issues with the “heme” portion or the “globin” portion

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24
Q

What are the reasons why an anemia may be normocytic?

A

anemia with normocytic cells means the RBC are normal-sized but there is a low # of them

↓ production or ↑ destruction or loss

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25
Q

What are the two types of macrocytic anemia? What is the difference?

A

Megaloblastic
Impaired DNA synthesis
Ex: B12, folate deficiency

Non-megaloblastic
Not caused by impaired DNA synthesis
Ex: liver disease

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26
Q

Megaloblastic anemia is due to…..

A

Impaired DNA synthesis

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27
Q

Non-megaloblastic anemia is due to……

A

Not caused by impaired DNA synthesis

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28
Q

Onset of Anemia

A

May be acute or develop slowly

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29
Q

What causes the signs and symptoms of anemia?

A

Signs & symptoms vary with degree of RBC reduction & how long it has been present

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30
Q

What is the end result of anemia?

A

End result is a decrease in the oxygen carrying capacity of the blood

Perfusion to nonvital tissues is compromised to sustain perfusion of vital organs

Initially patients be asymptomatic

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31
Q

What are the common symptoms of anemia?

A

Fatigue, dizziness, weakness, SOB, tachycardia
↓ mental acuity
Pallor, cold extremities

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32
Q

Diagnosis of anemia includes:

A

Medical History

Physical Examination

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33
Q

A medical history for the diagnosis of anemia depends on:

A

Past & current hgb & bloodwork if available

Comorbid conditions

Occupational, environmental & social history (menstrual cycle, alcohol, pregnancy)

Transfusion

Family history

Medications (antiretrovirals, immunosuppressants, cytotoxic, folate antagonists)

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34
Q

A physical examination for the diagnosis of anemia depends on:

A

Pallor

Postural hypotension, tachycardia (hypovolemia – acute blood loss)

Neurologic findings (B12 deficiency)

Jaundice? (hemolysis)

Bleeding gums, blood in stool, urine, epistaxis etc. (hemorrhage)

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35
Q

A complete blood count encompasses:

A

Hemoglobin (Hb)
Measures the amount of hemoglobin in the bloo

Hematocrit (Hct) – amount of packed red blood cells (%)
Packed cell volume

RBC count

RBC indices
MCV, MCH, MCHC

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36
Q

What does MCV mean?

A

MCV=mean corpuscular volume

Average RBC volume

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37
Q

What does MCH mean?

A

MCH=mean corpuscular hemoglobin

Ave mass of Hb/RBC

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38
Q

What does MCHC mean?

A

MCHC=mean corpuscular hemoglobin concentration

Average concentration of Hb within a volume of a packed volume of RBC. Shows colour

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39
Q

What is RDW?

A

RDW=Red blood cell distribution width

Measure in the variation of RBC width

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40
Q

What blood test informs one of RBC colour?

A

MCHC

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41
Q

Other laboratory evaluations that may be used for diagnosis?

A

RBC morphology

Reticulocyte count

Iron studies
Ferritin, serum iron, TIBC (total iron-binding capacity)

Peripheral blood smear

Stool for occult blood (G.I. Bleed, Cancer, marker for bleeding)

Bone Marrow aspiration and biopsy

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42
Q

The WHO defines anemia by…..

A

Anemia: Definition by hemoglobin

Men: <130 g/L
Women: <120 g/L

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43
Q

What are some specific types of anemia?

A

Deficiency-related anemias
Iron
Vit B12
Folate

Hemolytic anemia

Sickle cell anemia

Anemia related to other diseases/conditions
Anemia of chronic disease, CKD, critical illness/blood loss

Aplastic anemia

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44
Q

What is the most common nutritional deficiency worldwide?

A

Iron Deficiency

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45
Q

What are the sx of iron deficiency anemia?

A

Associated with symptoms of pallor, cardiovascular, respiratory and cognitive complications & decreased quality of life

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46
Q

Describe the general process of iron deficiency anemia

A

A negative state of iron balance in which daily iron intake are unable to meet RBC and other body tissue needs

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47
Q

What are some causes of iron deficiency anemia?

A

Lack of dietary intake
–> Vegetarians/vegans, poor diet

Blood loss
–> Menstruation, gastrointestinal (e.g. peptic ulcer), trauma

Decreased absorption
–> Celiac disease, medication, gastrectomy, regional enteritis

Increased requirement
–> Infancy, pregnant/lactating women

Impaired Utilization
–> Hereditary, iron use

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48
Q

What acronym can be used to describe the causes of iron deficiency?

A

Need – increased need as in pregnancy, children during stages of rapid growth, etc.

Intake is low, e.g. in malnutrition

Malabsorption

Blood

Loss, e.g. GI bleeding

Excessive donation, e.g. in blood donors

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49
Q

What is the relationship between iron-deficiency anemia and mortality?

A

Rarely a direct cause of death

Moderate-severe iron deficiency anemia can cause hypoxia –> aggravate underlying pulmonary/CV disorders

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50
Q

What is the relationship between iron deficiency anemia and morbidity?

A

Symptoms can be disruptive, impair daily functioning, etc

Slowed growth rate in children, ↓ ability to learn, lower IQ

Splenomegaly may occur with severe, persistent, untreated iron deficiency anemia

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51
Q

What is iron-deficiency anemia associated with in the elderly?

A

Anemia is associated with:

↑ risk of hospitalization and mortality
↓ quality of life
↓ physical functioning

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52
Q

What is iron-deficiency anemia associated with in the pregnant?

A

During pregnancy, anemia increases risk for:

low birth weights
preterm delivery
perinatal mortality

May be associated with postpartum depression

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53
Q

Describe the distribution of iron in the body

A

Body contains ~ 3-5g, of which 2g are found in Hg

Significant amount is stored as ferritin or aggregated ferritin (hemosiderin) in the liver, spleen, bone marrow

Small fraction in plasma, of which most is bound to transferrin (transport protein)

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54
Q

Describe iron stores in the body in comparison to RBC lifespan

A

Despite constant turnover of rbc, iron stores are usually well preserved

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55
Q

What controls iron metabolism?

A

Iron metabolism is regulated by hepcidin (hormone produced by liver, promotes storage)

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56
Q

Describe iron absorption in the body

A

Fe3+ (ferric) iron is ingested in the diet

Ionization in the stomach and reduction to Fe2+

Fe2+ (ferrous) iron is absorbed from the duodenum and upper jejunum by active transport

Fe2+ binds to transferrin (transport protein)

Incorporation into hemoglobin or stored as ferritin

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57
Q

Describe serum iron lab value. What lab value measures it?

A

Concentration of iron bound to transferrin.

Best interpreted in context with TIBC; fluctuate, subject to individual diurnal variation & may remain in normal range when iron stores are dropping

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58
Q

Describe ferritin lab value. Is it beneficial or detrimental to lab values?

A

‘Storage iron’

Most sensitive but non-specific and is elevated in inflammatory conditions, liver disorders etc.

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59
Q

Describe the TIBC (total iron binding capacity).

A

Indirect measurement of iron-binding capacity of transferrin, performed by adding an excess of iron to plasma to saturate and then removing the excess

Serum transferrin receptor levels , which reflect the amount of RBC precursors available for active proliferation are increased in iron deficiency anemia

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60
Q

Describe tsat (% transferrin saturation)

A

A measure of how much serum iron is actually bound

Serum iron ÷ TIBC x 100

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61
Q

If someone had low iron stores, what is there TIBC?

A

Low iron stores, high TIBC

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62
Q

In Iron deficiency anemia, what changes in lab values are noted? RBC morphology?

A

See decreases in:
- Ferritin
–> most sensitive marker but also non-specific
- serum iron
- transferrin saturation
- Hb and Hct (decline later – takes time for this to happen)

See increases in:
- total iron-binding capacity (increase in TIBC)

RBC morphology (takes time)
- Microcytic (↓ MCV)
- Hypochromic (↓ MCHC)

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63
Q

What are the two types of iron? What is the difference between them?

A

Heme iron
Derived from animal proteins
Better absorbed, more consistent absorption (~23% more)
Less affected by dietary factors

Non-heme iron
Plant sources
Fruits and vegetables, nuts, beans, grains, iron-fortified foods/supplements
Requires acidic GI pH for absorption

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64
Q

What can decrease the absorption of iron?

A

Phytates (grains, brans)

Polyphenols/tannins (coffee/tea)

Calcium (others too)

H2RAs (antagonism), PPIs

Gastrectomy/bariatric surgery/achlorhydria

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65
Q

What can increase the absorption of iron?

A

Increased stomach acidity (increase conversion of form)

Eating heme and non-heme sources at the same time

Cook with cast-iron or stainless steel pots/pans (↑ the amount of non-heme iron)

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66
Q

What are some people who require more dietary intake of iron?

A

Endurance athletes, pregnant

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67
Q

What is the dietary intake of iron for pregnancy?

A

RDA - 27 mg/day

Vegetarian - 49 mg/day

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68
Q

The diagnosis of iron-deficiency anemia is based on:

A

Symptoms
Medical history
CBC, labs, morphology

69
Q

What are the sx of iron deficiency anemia?

A

“Typical” anemia symptoms

Other symptoms
Brittle, spoon-shaped nails
Pica
Pagophagia
Smooth tongue

70
Q

When analyzing the medical history for iron-deficiency anemia, one should analyze…..

A

Pregnancy

NSAID Use (possible GI bless)

Diet

71
Q

What are the formulations of iron available?

A

Oral
Safe, convenient, cheap
Generally first line
–> Tablets
–> liquid

Parenteral iron therapy
–> Only used if needed

72
Q

What type of iron is often used for oral iron supplementation?

A

Generally see ferrous (Fe2+) salt forms used

73
Q

What is the adult dosing of oral iron supplementation?

A

~105-200 mg elemental Fe/day

74
Q

Should a pharmacist recommend SR or ER irron?

A

Don’t go for the hype of “enteric coated” or “SR”

–> don’t dissolve much until they reach the small intestine
–> significantly ↓ iron absorption, especially when used in patients with ↓ gastric acidity

75
Q

What are the available forms of iron available?

A

All Fe2+ supplements are absorbed similarly but each ferrous salt form contains varying amounts of elemental Fe

76
Q

What source are iron supplementation? Which ones should not be recommended and why?

A

Supplements are usually non-heme sources(exc. heme complex)

Polysaccharide & polypeptide complexes : expensive, benefits over cheaper formulations not shown to date

77
Q

What are some side effects of oral iron supplementation?

A

NV, constipation (sometimes diarrhea) – dose related

dark stools (warn patients)

78
Q

How should one take oral iron supplementation?

A

remembering to take on empty stomach

Make sure patients know how to take iron in relation to other meds, etc (and why!)

avoiding interactions with other foods/drinks/meds/minerals, etc

79
Q

How long should the length of therapy be for oral iron supplementation?

A

Need to take it for an extended period of time

80
Q

What is a critical part of counselling for oral iron supplementation?

A

Keep out of reach of children

NOTE: iron overdose in children is toxic

Counsel patients to keep iron supplements away from toddlers & children

Double check pediatric concentrations and dosages prior to dispensing

81
Q

What is the pediatric dosing of oral iron supplementation?

A

weight-based

depending on severity of anemia

3-6 mg/kg/d divided tid

Always double check the dose of iron supplementation

82
Q

What is a critical counselling point for oral iron liquid?

A

Iron may stain teeth

Mix liquid forms with juice or water to prevent staining of teeth

Use a straw, rinse with water after

83
Q

What are the sx of iron poisoning?

A

Sx’s usually become evident within 6 hours
Severe vomiting
Diarrhea
Abdominal pain
Dehydration and lethargy if not treated adequately
A child’s vomit or stool may be bloody.

84
Q

What is the treatment of iron poisoning?

A

Deferoxamine can be used to bind up excess iron

85
Q

How can a pharmacist make iron supplementation easier for a patient?

A

Lower the dose
–> Will take longer to correct anemia, but still works
–> Every other day dosing could be considered

Use small initial dose and gradually increase
–> Builds tolerance

Alternate day dosing
–> Single oral doses on alternate days

Take it with food
–> May affect absorption, but better than nothing
–> Consider vitamin C to increase absorption

Take it before bed
–> “sleep off” bothersome s/e

86
Q

Parenteral Iron Supplementation Route of Admin

A

Given IV (IM route is no longer routinely used)

Quicker hematologic response than that of oral iron

87
Q

When is parenteral iron supplementation used?

A

evidence of iron malabsorption

intolerance to oral iron

long-term non-adherence to oral therapy

excessive iron loss

88
Q

What are the parenteral formulations of iron and its respective amount of iron?

A

Iron dextran (Infufer®)
50mg elemental Fe/ml
Discontinued

Iron sucrose (Venofer®)
20mg elemental Fe/ml

Iron sodium ferric gluconate (Ferrlecit®)
12.5mg/ml

Iron Isomaltoside (Monoferric®)
100,mg/ml

89
Q

What is the dosing of parenteral iron? What are the risks/s/e? How are they diminished?

A

Various dosing strategies used

Risk of anaphylaxis

Other s/e:
–> systemic rxns (myalgias/arthralgias), h/a, NV, flushing, itching, fever, injection-site reactions

Can be diluted in NaCl and given via slow infusion to decrease risk of reactions

90
Q

What is the rate of hemoglobin concentration increase when iron supplementation occurs?

A

Hb concentrations increase at a rate of ~10g/L per week

91
Q

When is anemia usually corrected by? How long should therapy for iron

A

Anemia is usually “corrected” by 6 wks

Need to continue tx for at least 3 months after the anemia is resolved

Allow for repletion of iron stores and to prevent relapse
Monitor via ferritin

92
Q

What is the function of Vitamin B12?

A

Vitamin B12 (cobalamin) is required for proper red blood cell formation, neurological function, and DNA synthesis

93
Q

How is Vitamin B12 produced?

A

The body can’t make it; must be consumed (microbe production is not sufficient for the body)

94
Q

Where is B12 stored? How long does it take to become deficient?

A

Large stores in the liver & low daily requirements

Deficiency develops over many years

95
Q

What are some sources of vitamin B12?

A

Everything that walks, swims or flies contains vitamin B12. Nothing that grows out of the ground contains vitamin B12…unless fortified

fish, meat, poultry, eggs, milk and milk products
Fortified foods ex) breakfast cereals
Nutritional yeast products
Supplements (usually present as cyanocobalamin)

96
Q

What is the dietary intake of B12 for adults (14+)?

A

2.4 mcg

97
Q

What is the B12 recommendation dietray intake for pregnancy and lactation?

A

Pregnancy - 2.6 mcg
Lactation - 2.8 mcg

98
Q

Describe the process of B12 absorption in the body

A

HCl acid & gastric protease in stomach releases B12 bound to protein in food
–> synthetic vitamin B12 is already in “free form”

Free B12 combines with intrinsic factor (IF)
IF: a glycoprotein secreted by parietal cells of the stomach (Transport protein)

The IF is discarded in the terminal illeum and the B12 is bound to a transport protein (transcobalmin II) for secretion into the blood

Absorption is generally poor

Some B12 can be absorbed via diffusion (alternate pathway – only 1%)

99
Q

What is the extent of B12 absorption in the body?

A

Absorption is generally poor

100
Q

What is the importance of the B12 diffusion mechanism of absorption?

A

Important only when large amounts of B12 are ingested
Provides only small amounts of B12

101
Q

What happens to B12 absorption when capacity of IF is exceeded?

A

Absorption ↓ significantly when the capacity of IF is exceeded

102
Q

What is the rate-limiting process of B12 absorption?

A

Absorption ↓ significantly when the capacity of IF is exceeded

103
Q

What are some causes of B12 deficiency?

A

Inadequate intake
–> Vegans (more of an animal source), low socioeconomic status, elderly (may not have the best diet, may not eat as much)

Malabsorption
–> Age
Atrophic gastritis (10%–30% of older adults) ↓ HCl secretion in stomach (can still absorb supplemental B12)
–> Pernicious anemia
–> gastrectomy, bariatric surgery, achlorhydria, small bowel disorders, drugs

Inadequate utilization (bound to transcolbomin –> may be inhibited)

104
Q

What is pernicious anemia?

A

autoimmune disease that affects the gastric mucosa

–> Intrinsic factor deficiency

105
Q

What is the result of pernicious anemia?

A

destruction of parietal cells

achlorhydria

failure to produce IF

106
Q

What is the relationship between pernicious anemia and B12? Risks?

A

Malabsorption of B12, even with appropriate dietary intake

Associated with increased risk of gastric cancer

107
Q

What are the typical symptoms of pernicious anemia?

A

Typical anemia sx (lethargy, palour, etc)

Often neurological (can be severe)
numbness/tingling in the hands and feet – usually bilateral
difficulty maintaining balance
depression, confusion, dementia, poor memory

–> Can lead to dymyelination of the nerves and spinal cord –> SLowed brain development in children

Soreness of the mouth or tongue

108
Q

Why is it important to diagnose B12 and treat early?

A

Neurological symptoms of vitamin B12 deficiency can occur without anemia (may not see blood parameters)

Neurological sx are often progressive and can be irreversible (diagnose and tx early)

109
Q

When gathering a history for pernicious anemia, one should investigate?

A

Diet

Age

Any GI surgery, intestinal disease, etc

Med use (potentiate B-12 deficiency)

H2RAs, PPIs –> Decrease stomach acidity, decrease absorption

Colchicine – induce reversible vitamin B12 absorption by altering the function of the mucosa of the small intestine

Metformin – Diabetes – Lead to deficiency

110
Q

If someone has type 2 diabetes, why should a pharmacist monitor B12?

A

Want to check vit B12 as see peripheral neuropathy

Rule out B12 anemia

111
Q

What lab value and morphology changes are seen in B-12 deficiency anemia?

A

See decrease in:
–> serum or plasma vitamin B12 levels

See increase in:
–> serum homocysteine level (early)
–> Methylmalonic acid (MMA) levels

To check for pernicious anemia
–> Schilling test, antibodies to IF/parietal cells

RBC:
macrocytic (↑ MCV)
normochromic (normal MCHC)

112
Q

What is a critical enzymatic process that involves B12?

A

MMA & Homocysteine are involved in enzymatic reactions that depend on vitamin B12

B12 is a cofactor for L-methymalonyl CoA

B12 and folate are co-factors for methionine synthetase

Succinyl CoA is required for protein and fat metabolism as well as hemoglobin synthesis

Both processes are required for the production of SAMe (s-adenosyl methionine) which is a universal donor for many essential rxn’s in the body

113
Q

Why is it important that we treat B-12 deficiency?

A

In infants
failure to thrive, movement disorders, developmental delays

Irreversible neurological damage

↑ homocysteine levels are a risk factor for CV disease, some links to Alzheimer’s

114
Q

What are the goals of therapy for B12 deficiency?

A

Correct underlying cause (if possible)
Replenish stores (b12 Supplementation)
Reverse symptoms (or slow progression if irreversible)

115
Q

What are the types of B12 supplementation available? What formulations?

A

Most common form cyanocobalamin (synthetic); others are hydroxycobalamin or methylcobalamin (no evidence that one is better than the other)

Oral
IM

116
Q

Can high doses of B12 be given. If so, why?

A

Can give high doses as B12 is non-toxic

117
Q

What is the treatment of B12 deficiency anemia if dietary and no pernicious anemia? Exception?

A

For treatment in pts with deficiency not related to pernicious anemia
–> 100 ug daily orally has been shown to normalize B12 levels within one month

Now sometimes used even in pts with impaired absorption
~1% of an oral dose of B12 can be absorbed by non-IF process

118
Q

When is IM B12 supplementation used? What are some disadvantages?

A

More commonly used if:

Pernicious anemia
Severe malabsorption issues
Non-adherence with oral therapy
Neurologic symptoms (until resolution)

More expensive, inconvenient, injection related s/e

119
Q

B12 deficiency (e.g. diet) dosing

A

Initial treatment:
30 ug daily SC/IM × 5–10 daysor 500-2000 ug daily PO

Life-long maintenance:
100–200 ug monthly SC/IMor250 ug daily PO

120
Q

Pernicious Anemia/Other chronic malabsorption disorders treatment

A

B12 Supplementation

Initial treatment:
100 ug daily SC/IM × 1 wk; 200 ug weekly SC/IM until Hb normalizes

Life-long maintenance:
100 ug monthly SC/IMOR 1000–2000 ug daily PO

121
Q

What is folate?

A

Water-soluble B vitamin

Easily destroyed by cooking or processing

122
Q

What is folate deficiency anemia? How is folate stored? When does anemia become present?

A

The body can’t make enough to meet daily needs

Consume in foods/supplements

~4-6 mos supply stored in liver (may deplete in 6wks if diet is severely deficient)

123
Q

Where is folate absorbed? Which type absorbs more extensively?

A

Absorbed in the small intestine

Synthetic FA absorbs better than food-source folate

124
Q

Why is folate important?

A

Tetrahydrofolate (THF) is a cofactor in DNA synthesis, metabolism of homocysteine

Folate also important to prevent neural-tube defects

125
Q

What are some sources of folate?

A

Good dietary sources:
leafy green vegetables (spinach)
fruits (citrus fruits and juices)
dried beans and peas
beef liver
fortified cereals (contain folic acid instead of folate)

Supplements (folic acid)

126
Q

What is the recommendation of folate for 14+?

A

400 mcg/day

127
Q

Folate recommendation for pregnancy and lactation

A

Pregnancy - 600 mcg/day

Lactation - 500 mcg/day

128
Q

What are some causes of folate deficiency?

A

Inadequate intake
Common –> elderly, fad dieters, alcohol use disorder, low SES

Increased requirements
Pregnancy (needs may triple)

Malabsorption

Certain drugs
May reduce absorption or alter metabolism

129
Q

When is more folate required for a person?

A

Need increased requirements whenever there is more cellular division –> inflammation, pts who have burns, growing adolescants (rapid cell turnover)

130
Q

What are some drug causes of folate deficiency?

A

Anticonvulsant medications: phenytoin, primidone, phenobarbital, carbamazepine, valproic acid
–> Affect folate absorption and/or cell utilization

Metformin

Methotrexate – high doses in oncology, supplement

Sulfasalazine

Triamterene

Trimethoprim (as found in cotrimoxazole)

131
Q

What are the sx of folate-deficiency anemia?

A

similar to those seen with B12 deficiency but without neurological sx

132
Q

What lab value and morphology changes are noticed in folate-deficiency anemia?

A

Labs:
↓ serum folate (may sometimes be WNL)
Order RBC folate
↑ homocysteine levels
Always check B12 levels!

RBCs:
Macrocytic, normochromic (indistinguishable from B12 deficiency)

133
Q

Why should a folate deficiency be treated?

A

Pregnancy
low birth weight, prematurity
neural tube defects

Children
slow overall growth rate

General morbidity related to anemia

134
Q

What is the treatment of folate deficiency? WHo should get it?

A

Give oral supplementation, even in patients with absorption problems.

Folic acid should be given for confirmed folate deficiency, pregnancy or in situations of increased demand, such as hemolysis.

135
Q

What is the dose of treatment for folate deficiency?

A

1mg/day folic acid usually sufficient

5mg/day (Rx) if absorption compromised or drug-induced deficiency

136
Q

How long should folate deficiency be treated for?

A

4 mos to allow all folate-deficient RBCs to be cleared from the circulation (RBC cycle is 120 days)
–> May continue long-term (drug-induced, malabsorption)
–> Correct diet

137
Q

If someone has a folate deficiency and a concurrent B12 defeciency, what are the steps of action? What is a concern?

A

symptoms of anemia will improve and a partial hematologic response will occur with folate replacement

BUT the neurologic issues related to B12 deficiency will not be reversed by folate (may “mask” a B12 deficiency)

138
Q

What is the monitoring plan for B12 and folic acid?

A

Reticulocyte response within 3–4 days
Hb improving by ~ day 10
Full resolution of the anemia ~ 2 months
Neurologic deficits with B12 may take 6 months or longer

The rapid production of new hematopoietic cells leads to a potentially dramatic shift of K from extracellular to intracellular compartments, which may cause profound hypokalemia.

–> Watch older patients on diuretic therapy for heart failure
–> If at risk, obtain a baseline K level and give K supplementation in patients with low or borderline potassium levels.
–> Monitor K levels in the first few days of therapy and adjust accordingly

139
Q

What is hemolytic anemia?

A

Decreased survival time of RBCs secondary to destruction in the spleen or circulation

RBC lifespan can be as short as 5 days!

Can be an acute event or chronic, mild to severe

140
Q

In hemolytic anemia, what is the RBC morphology?

A

Usually normocytic and normochromic

Increased levels of reticulocytes

141
Q

What are the causes of hemolytic anemia?

A

Often idiopathic

Can be caused by immune reactions, malignancy, drugs (~10%)

G6PD enzyme deficiency
–> Inherited defect (x chormosme, males)
–> Normally protects RBCs against oxidative stress
–> More susceptible to triggers –> Chloroquine, nitrofurantoin, SMX

142
Q

What are some drugs that can cause hemolytic anemia?

A

ACE-I, NSAIDs/ASA, antibiotics (pens/cephs/tetracycline/levofloxacin/sulfonamides)

143
Q

What is the treatment of hemolytic anemia?

A

correcting or controlling the underlying cause

steroids and other immunosuppressive agents have been used for management of autoimmune hemolytic anemias

splenectomy is sometimes indicated in an attempt to reduce RBC destruction

144
Q

What is sickle-cell anemia?

A

Autosomal recessive Hgb disorder characterized by a DNA substitution at the β-globulin gene

145
Q

What is the pathology of sickle cell anemia?

A

Results in an abnormal type of Hb called hemoglobin S

HbS distorts the shape of RBC, especially when exposed to low oxygen levels

Sickled RBCs are rigid and do not pass through microvasculature, prone to rupture
–> Ischemia, pain
–> Chronic organ damage

146
Q

What are some symptoms of sickle cell anemia?

A

Impaired growth and development

Enlarged spleen

Chronic damage to many organs (fibrosis)

Vaso-occlusive crises
–> “Sludging” of sickled cells in microvasculature
–> Often occur with exposure to heat/cold, exercise, infection, stress, high altitude
–> Pain in bones of the back, long bones, chest

147
Q

What lab value changes and RBC morphology changes are noted in sickle-cell anemia?

A

Labs:
Hb electrophoresis –> HbS present

RBC:
Normochromic, normocytic
Presence of sickled cells

148
Q

What is the treatment for an acute episode of sickle-cell anemia?

A

Acute episodes: pain meds, hydration (eliminate trigger)

Vaccinations & Penicillin prophylaxis for children up to age 6
–> Protects against encapsulated bacteria such as Streptococcus Pnuemonia or Hemophilus influenzae.

149
Q

Pharmacological/Medical Tx of Sickle Cell Anemia

A

Hydroxyurea
–> seems to work by stimulating production of fetal Hb
–> HbF helps prevent the formation of sickle cells
–> concern re tumors/leukemia with long-term use

Partial blood-transfusions

Bone-marrow transplant
curative, but has its own set of risks

150
Q

What is anemia of inflammation?

A

Anemia of Inflammation is a term used to describe both anemia of chronic disease, and anemia of critical illness

Reflects inflammatory process resulting in disturbances in iron homeostasis underlying both types of anemia

151
Q

How is anemia of a chronic disease diagnosed?

A

A diagnosis of exclusion

152
Q

What are the causes of anemia of a chronic dx?

A

chronic inflammation, infection, or malignancy
–> Can occur as early as 1 to 2 months after the onset of these processes (can be later)
–> Exact mechanisms unclear
–> Treatment is aimed at correcting the underlying pathology

153
Q

What are the symptoms of anemia of a chronic disease?

A

may be mild, non-specific

154
Q

What lab value and RBC morphology changes noticed in anemia of a chronic dx?

A

Labs:
↓ Hct
↓ serum iron but normal or ↑ ferritin and normal or ↓ TIBC

RBC morphology:
Usually normocytic and normochromic (can be microcytic)

155
Q

Contrast anemia or a chronic disease and iron deficiency anemia (Serum Ferritin, Serum iron, Tsat, TIBC, Hb)

A
156
Q

What is anemia due to CKD?

A

Erythropoiesis is decreased

Uremic metabolites ↓ the life span of circulating RBCs

157
Q

What are the sx of anemia due to CKD?

A

general anemia sx, angina, ischemia on ECG, CHF (new-onset or worsening)

158
Q

What is the treatment of anemia due to CKD?

A

Iron
Erythropoetin Stimulating Agents
–> Erythropoeitin, darbepoeitin
Transfusions

159
Q

In what patients are erythropoetin stimulating agents used?

A

Patients with chronic renal failure
HIV-infected patients receiving antiretroviral therapy
Chronic hepatitis C patients receiving ribavirin
Patients receiving chemotherapy for nonhematologic cancers
Surgery patients
Patients with low-risk myelodysplastic syndrome

160
Q

What is anemia in the critcially ill? What are some contributing factors?

A

Body trying to heal, increased demands

Found almost universally in this patient population

161
Q

Anemia in the critically ill lab value changes?

A

DECREASES IN:

serum iron, TIBC, iron/TIBC ratio
serum ferritin is normal to high

162
Q

What is aplastic anemia? What do you see?

A

Failure of pluripotent stem cells in bone marrow

Hematopoiesis is interrupted

See anemia (RBC), neutropenia (WBC), thrombocytopenia (platelets)

163
Q

What are the causes of aplastic anemia?

A

70% idiopathic

Can be related to toxicity from drugs/chemicals, congenital defect, viruses

Allopurinol, chloramphenicol, NSAIDS, sulfonamides, chemo drugs

Immune-mediated suppression of stem cell function

164
Q

How is aplastic anemia diagnosed?

A

Defintive Diagnosis
–> Abnormal bone marrow biopsy
–> usually see 30-70% of blood cells should be stem cells but here replaced by fat

165
Q

What are the sx of aplastic anemia?

A

variable; depends on which cell line is affected the most
Anemia sx (fatigue, pallor, etc)
Bleeding
Fever, infection

166
Q

What lab value changes do you see with aplastic anemia?

A

Normochromic, normocytic RBC
Very low blood counts

167
Q

What is the treatment of aplastic anemia?

A

Supportive care, Removal of causative agent

Bone-marrow transplant or Immunosuppression if not possible

168
Q

Describe the different types of anemia by their effect on RBC morphology

A

PHAR 253 Final (8 decks)

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