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Therapeutics Module 3 > Anemia > Flashcards

Anemia Flashcards

1
Q

What is the definition of Anemia?

A

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

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2
Q

What does anemia result in?

A

Decreased oxygenated blood carrying capacity

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3
Q

Where are RBCs developed? Adult/Child

A
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4
Q

What are the components of RBC?

A

Hemoglobin taht contains protein component and heme component

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5
Q

What is erythropoiesis?

A

Works on a feedback loop
– ↓ tissue oxygen concentration signals the kidneys to ↑ production and release of EPO

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6
Q

What does Erythropoiesis do?

A

lStimulates stem cels to differentiate

Increase release of reticulocytes from bone marrow

Induces HB formation

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7
Q

What are the 3 main causes of anemia?

A

Blood loss
Inadequate RBC production
Excessive RBC destruction

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8
Q

What are the three different sizes of RBC morphology?

A

Microcytic, Normocytic, Macrocytic

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9
Q

What are the three different colours of RBC?

A

Hypochromic
Normochromic
Hyperchromic

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10
Q

If considered less then <80 fl what is the relative size?

A

Microcytic or small

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11
Q

If considered between 80-100 fl what is the relative size?

A

Normocytic

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12
Q

If considered less then >100 fl what is the relative size?

A

Macrocytic

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13
Q

What is colour reflected in with respect to RBC?>

A

by the mean corpuscular Hb concentration

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14
Q

What is the primary cause of microcytic based RB? (2)

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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15
Q

What does normocytic anemia mean?

A

RBC are
normal-sized but there is a low # of them
– ↓ decreased production or ↑ destruction or loss

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16
Q

With respect to macrocytic what can the RBC be?

A

Megaoblastic or Non-Megablastic

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17
Q

What is megaloblastic RBCs? Caused by?

A

–mpaired DNA synthesis – Ex: B12, folate deficiency

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18
Q

What is Non-megaloblastic RBCs? Caused by?

A

Not caused by impaired DNA synthesis

Liver disease

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19
Q

What is the general onset of anemia?

A

May be acute or develop slowly

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20
Q

What is the end result in anemia?

A

Decrease in the oxygen carrying capacity of the blood

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21
Q

Common symptoms of anemia?

A

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

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22
Q

What is the diagnosis of anemia usually include?

A

Medical history
Physical exam
Lab Evaluation

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23
Q

What things the medical history are we looking for?

A

– Past & current hgb & bloodwork if available
– Comorbid conditions
– Occupational, environmental & social history
– Transfusion
– Family history
– Medications

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24
Q

What things in the Physical examination are we looking for?

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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25
Q

What lab values are we investigating with respect to Complete blood count

A

Hb
Hematocrit
RBC count
RBC indices

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26
Q

What is Hematocrit?

A

Packed cell volume

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27
Q

What is the RBC indicies MCV?

A

Mean Corpuscular Volume

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28
Q

What is the RBC indicies MCH?

A

Mean corpuscular hemoglobim

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29
Q

What is the RBC indicies MCHC?q

A

Mean corpuscular hemoglobin concentration

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30
Q

What is the RBC indicies RDW

A

Red blood cell distribution width

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31
Q

What is Mean Corpuscular hemoglobin

A

Average amount of hemoglobin in each RBC

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32
Q

According to WHO what is ocnsidered low hemoglobin?

A

Men <130
Women <120

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33
Q

What is iron deficient 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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34
Q

What are the causes of Iron Deficient Anemia?

A

Lack of Dietary intake
Blood loss
Decrease absorption
Increased requirement
Impaired utilization

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35
Q

What is the Acronym NIMBLE stand for?

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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36
Q

Why do we treat Iron deficient anemia?

A

Low risk of mortaility, but can cause or aggravate underlying pulmonary/CV dosirders

Morbidity, May impair daily functiontining. Slowed growth rate in children and decreased ability to learn

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37
Q

What is Splenomegaly?

A

Enlarged spleen

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38
Q

What is Anemia associated with in elderly?

A

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

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39
Q

In pregnancy anemia increases risk for?

A

Low birth weights
Preterm delivery
Perinatal Mortality

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40
Q

How muhc iron does our body contain?

A

3-5g with 2g found in Hg

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41
Q

What form is iron usually storred as?

A

Ferritin or aggregated ferritin in the liver spleen and bone marrow

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42
Q

Where is a small fraction of iron storred?

A

Plasma which most is bound to transferrin

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43
Q

What is serum iron?

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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44
Q

What is ferritin?

A

– ‘Storage iron’
– Most sensitive but non-specific and is elevated in inflammatory conditions, liver disorders etc.

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45
Q

What is the definition of TIBC?

A

Total iron binding capacity

– Indirect measurement of iron-binding capacity of transferrin, performed by adding and 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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46
Q

What is Tsat?

A

(% transferrin saturation)

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47
Q

What is tsat define?

A

– A measure of how much serum iron is actually bound – Serum iron ÷ TIBC x 100

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48
Q

In iron deficiency anemia what are we expecting to see with respect to decreases?

A

Ferritin
Serum Iron
Transferrin saturation
Hb and Hct (Decline later)

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49
Q

What do we expect to see increases in with respect to iron deficiency anemia?

A

Total iron binding capacity

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50
Q

What is the general RBC morphology in Iron deficient anemia?

A

– Microcytic (↓ MCV)

– Hypochromic (↓ MCHC)

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51
Q

Where is Heme iron derived from?

A

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

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52
Q

Where is non-heme iron derived from>?

A

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

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53
Q

What decreases absorption of iron?

A

Phytates *Grains, brans)
Polyphenols/tannins (Coffee/tea)

Calcium

PPIs, H2RAs

Bariatric surgery

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54
Q

What increases iron absorption?

A

Stomach acidity
Eating heme and non heme soources at the same time

Cook with cast iron or stainless steel to increase the amount of non-heme iron

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55
Q

What are the three criteria assessed for iron deficiency anemia?

A

Based on:
– Symptoms
– Medical history
– CBC, labs, morphology

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56
Q

What are the other symptoms that may occur with iron deficient anemia?

A

– Brittle, spoon-shaped nails
– Pica
– Pagophagia
– Smooth tongue

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57
Q

What is PICA?

A

craving and chewing substances that have no nutritional value

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58
Q

What are the 2 formulations available for iron?

A

Oral and parenteral iron therapy

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59
Q

What is the general adult dosing of iron each day?

A

105-200mg elemntal per day

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60
Q

% of absorption of F Fumerate

A

33%

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61
Q

% of absorption of F Sulphate

A

20%

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62
Q

% of absorption of F Gluconate

A

11%

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63
Q

Whaat is the % of absorption of polysaccaride iron complex

A

Feramax 100%

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64
Q

Are supplements usually heme or non-heme sources?

A

Non-heme

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65
Q

What are some things to remember when taking iron?

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

66
Q

What is the length of therapy with iron?

A

– need to take it for an extended period of time

67
Q

What is the pediatric weight of iron dosing?

A

3-6 mg/kg/d divided tid

68
Q

What is important when using formulations for pediatrics?

A

DOUBLE CHECK CONCENTRATION

69
Q

What is iron dose lead to>?

A

In children it is toxic?

70
Q

Can iron stain teeth?

A

yEs

71
Q

What are the Sx’s of iron poisoning?

A

– Severe vomiting
– Diarrhea
– Abdominal pain
– Dehydration and lethargy if not treated adequately – A child’s vomit or stool may be bloody.

72
Q

What can Deferoxamine be used for?

A

Bind up excess iron in iron poisoning

73
Q

When is IV iron usually used?

A

– evidence of iron malabsorption
– intolerance to oral iron
– long-term non-adherence to oral therapy – excessive iron loss

74
Q

What is the formulations of IV iron?

A

Iron sucrose
Iron Sodium ferric gluconate
Iron Isomaltoside

75
Q

What is the risk of iron IV?

A

Anaphylaxis

76
Q

How long should be treat with iron?

A

Hb concetration increases at a rate of 10g/L per week

Anemia is corrected by 6 weeks

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

77
Q

How do we monitor anemia treatment?

A

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

78
Q

What type of chains are present in infants?

A

Gamma chains which allows for more oxygen to be carried

79
Q

What is the average RBC turnover?

A

120 days

80
Q

What happens with decreasing kidney function?

A

Anemia

81
Q

What is Hematocrit?

A

Percentage of RBC in body

82
Q

What is vitamin B12 required for?

A

proper red blood cell formation, neurological function, and DNA synthesis

83
Q

Can the body make vitamin B12?

A

NO

84
Q

How long does B12 deficiency take to develop?

A

Many Years

85
Q

Where can you find Vitamin B12?

A

Anything that walks swim or flies contains vitamin B12

86
Q

What is the required amount of B12 required in pregnancy?

A

2.6mcg

87
Q

What is the required amount of B12 required in Lactation?

A

2.8mcg

88
Q

How does B12 get broken down in the stomach?

A

HCL (Stomach acid)

89
Q

What is the gastric parietal cell?

A

These types of cellsl ive in the gut and they produce intrinsic factor?

90
Q

What is the prupose of intrinsic factor?

A

Combines with free b12 in its free form

91
Q

What happens once IF-B12 enters the terminal illeum?

A

the IF is discarded and the b12 is bound to a transport protein transcobalmin II for secretion into the blood

92
Q

What is the issue with B12 absorption

A

Generally poor

93
Q

When does absorption of B12 decrease?

A

When the capacity of IF is exceeded

94
Q

Who is at risk of decreased B12 absorption?

A

Vegans, elderly

95
Q

What happens if we do not have enough intrinsic factor?

A

This can lead to what we call pernicious anemia

96
Q

How does IF deficiency occur?

A

Autoimmune disease generally. Leading to malabsorption of B12

97
Q

What does IF deficiency result in physiologically

A

Destruction of parietal cells
Achlorhydria
Failure to produce IF

98
Q

What is Achlorhydria

A

A condition in which the stomach does not produce hydrochloric acid

99
Q

What occurs in B12 deficient anemia?

A

Typical anemia Sx

Numbness/tingling in hands and feet
Difficulty maintaining balance
Depression, confusion, dementia, poor memory

Mouth sores

100
Q

Neurological sx of B12 deficiency are often progressive and can be?

A

Irreversibly

101
Q

What can the labs tell us with B-12 deficiency?

A

B12 levels are low

102
Q

What labs in b12 deficiency will be increased?

A

– serum homocysteine level (early)
– Methylmalonic acid (MMA) levels

103
Q

What lab values will decrease in b12 deficiency

A

– serum or plasma vitamin B12 levels

104
Q

What will be the RBC presentation in B12 Deficiency?

A

– macrocytic (↑ MCV)
– normochromic (normal MCHC)

105
Q

What pathway is B12 involed in?

A

MMA –> Succinyl CoA

Homocysteine –> Methionine

106
Q

In infants why is it important to treat B12-Deficiency?

A

– failure to thrive, movement disorders, developmental
delays

Irreversible neurological damage

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

107
Q

What is the general treatments of B12 deficiency?

A

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

108
Q

What is B12 treatment in deficiency not related to pernicious anemia?

A

– 100 ug daily orally has been shown to normalize B12 levels within one month

109
Q

In patients with impaired absorption

A

~1% of an oral dose of B12 can be absorbed by non- IF process

110
Q

When is IM B12 supplementation generally used?

A

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

111
Q

What are the disadvantages of B12 IM

A

– More expensive, inconvenient, injection related s/e

112
Q

What is the initial treatment of B12-Deficiency?

A

B12 deficiency (e.g. diet)

  • Initial treatment:
    – 30 g ug daily SC/IM × 5–10 days or 500-2000 ug daily PO
113
Q

What is the Lifelong maintenance of B12 supplementaiton?

A

– 100–200 ug monthly SC/IM or 250 ug daily PO

114
Q

What is the intial treatment for Pernicious anemia or other chronic malabsorption disorders?

A

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

115
Q

What is the life long maintenance in pernicious anemia?

A

– 100 ug monthly SC/IM OR 1000–2000 ug daily PO

116
Q

What is folate?

A

Water soluble B-Vitamin

117
Q

How much folate is generally stored in the liver?

A

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

118
Q

Where is folate absorbed

A

– Synthetic FA absorbs better than food-source folate

119
Q

What is the importance of Folate?

A

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

Folate also important to prevent neural-tube defects

120
Q

What are good dietary sources of folate?

A

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

121
Q

What is the needed folate intake in pregnancy?

A

600ug

122
Q

What is the needed folate intake in lactation

A

500

123
Q

Causes of folate deficiency

A

Inadequate intake
Increased requirements
Malabsorption
Certain Drugs

124
Q

Drugs that cause folate deficiency

A
  • Anticonvulsant medications: phenytoin, primidone, phenobarbital, carbamazepine, valproic acid
    – Affect folate absorption and/or cell utilization
  • Metformin
  • Methotrexate
  • Sulfasalazine
  • Triamterene
  • Trimethoprim (as found in cotrimoxazole)
125
Q

What are the symptoms of Folate related deficiency?

A

Similar to those seen with B12 Deficiency but without neurological symptoms***

126
Q

What are the lab related values evaluated in folate deficient anemia?

A

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

127
Q

What is decreased in folate deficiency related anemia?

A

Serum folate

128
Q

What is increased in folate deficient anemia?

A

Homocysteine levels

129
Q

What is the RBC presentation in folate deficient anemia?

A

Macrocytic, normochromic (indistinguishable from B12 deficiency)

130
Q

What pathway does folate take part in?

A

Homocysteine to methionine

131
Q

Why do we treat folate deficient anemia in pregnancy?

A

– low birth weight, prematurity
– neural tube defects

132
Q

Why do we treat folate deficient anemia in Children?

A

Slow overall growth rate

133
Q

What is the treatment dose of folate deficient anemia?

A

– 1mg/day folic acid usually sufficient

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

134
Q

What is the duration of folate deficient anemia treatment?

A
  • 4 mos to allow all folate-deficient RBCs to be cleared from the circulation

– May continue long-term (drug-induced,malabsorption)

– Correct diet

135
Q

What occurs with concurrent B12 Deficiency?

A

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

136
Q

Will folate reverse B12 deficiency related neurological issues?

A

No, instead it may mask a B12 deficiency

137
Q

What is hemolytic Anemia?

A

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

138
Q

What is the RBC lifespan in Hemolytic anemia>

A

RBC lifespan can be as short as 5 days!

139
Q

What is the presentation of RBC in Hemolytic anemia?

A

– Usually normocytic and normochromic
– Increased levels of reticulocytes

140
Q

What is the cause of hemolytic anemia?

A

Idiopathic
Immune reactions
Drug induced

141
Q

Which enzyme may cause hemolytic anemia?

A

G6PD enzyme deficiency

142
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

143
Q

What is the causes of Sickle Cell anemia?

A
  • Autosomal recessive Hgb disorder characterized by a DNA substitution at the β-globulin gene
144
Q

What is the abnormal HB called in Sickle Cell anemia?

A

Hemoglobin S

145
Q

Symptoms of Sickle Cell anemia?

A

– Impaired growth and development
– Enlarged spleen
– Chronic damage to many organs

146
Q

How is sickle cell anemia diagonised?

A

– Hb electrophoresis→HbS present

147
Q

What is the RBC presentaiton in sickle cell anemia?

A

– Normochromic, normocytic – Presence of sickled cells

148
Q

What is the treatment of sickle cell anemia?

A

Treat as symptoms occur

149
Q

What is hydroxyurea treatment?

A

– 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

Sickle Cell Anemia

150
Q

What is the presentaiton of Anemia of chronic disease?

A

– may be mild, non-specific

151
Q

What are the labs of Anemia of chronic disease?

A

– ↓ Hct
– ↓ serum iron but normal or ↑ ferritin and normal or ↓ TIBC

152
Q

In Anemia of chronic disease what is Serum Ferritin, Serum Iron, TSAT, TIBC and HB?

A
153
Q

In Iron deficient anemia what is Serum Ferritin, Serum Iron, TSAT, TIBC and HB?

A
154
Q

In anemia of critically ill patients what do we see decreases in?

A

– serum iron, TIBC, iron/TIBC ratio

– serum ferritin is normal to high

155
Q

What is the treatment of Anemia in critically ill?

A

– address cause
– exogenous EPO may/may not improve clinical outcomes

156
Q

What is aplastic anemia?

A
  • Failure of pluripotent stem cells in bone marrow * Hematopoiesis is interrupted
    – See anemia (RBC), neutropenia (WBC), thrombocytopenia (platelets)
157
Q

What are the Aplastic Anemia symptoms

A
  • variable; depends on which cell line is affected the most
    – Anemia sx (fatigue, pallor, etc)
    – Bleeding
    – Fever, infection
158
Q

What is the treatment of Aplastic Anemia?

A

– Supportive care, Removal of causative agent

– Bone-marrow transplant or Immunosuppression if not possible

159
Q

What are microcytic RBC presentations for which anemias?

A

– Iron deficiency, thalassemia,
anemia of chronic disease

160
Q

What are the normocytic anemia presentations?

A

– Sickle cell anemia, hemolytic anemia, aplastic anemia, anemia of chronic disease, anemia due to CKD, mixed deficiency anemias

161
Q

What are the macrocytic anemia presentations?

A

–B12/folic acid deficiency, liver disease

Therapeutics Module 3 (6 decks)

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