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PHARM 220 > Anemia > Flashcards

Anemia Flashcards

1
Q

Anemia Definition

A
  • When blood has a reduced capacity to delivery oxygen
  • reduced Hct, Hgb, or RBC count -> at least 1 of these = anemia
  • Males: Hgb<130 g/L
  • Females: Hgb <120g/L
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2
Q

Anemia triad

A
  1. Blood loss
  2. RBC destruction
  3. Inadequate production of normal RBCs
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3
Q

T or F: Anemia is a disease

A

False - Anemia is NOT a disease itself but a characteristic of underlying disorders

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4
Q

Conditions leading to Anemia Triad

A
  • Blood loss – heavy periods, ulcers, surgery, pregnancy
  • RBC destruction – kidney disease w/ dialysis, hemolytic anemia
  • Inadequate RBC – diet low in iron/folic acid/B12, sickle cell anemia, lack of EPO, pregnancy
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5
Q

Acute vs. Chronic Anemia Symptoms

A

Acute:
* Tachycardia, palpitations
* Hypotension, light-headedness
* Dyspnea (shortness of breath)

Chronic:
* Weakness, fatigue
* HA, vertigo, faintness
* Sensitivity to cold, pallor, loss skin tone

When Hgb <90g/L:
* Tongue pain, smooth tongue, pica, pagophagia

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6
Q

What Hormone Triggers RBC production?

A
  • Erythropoietin (EPO)
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7
Q

Where does Erythropoiesis Occur?

A
  • bone marrow
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8
Q

Normal Lifespan of RBC

A
  • 120 days
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9
Q

At what stages of differentiation is EPO important?

A
  • Erythroid burst-forming unit -> Erythroid colony-forming unit
  • Erythroid colony-forming unit -> Proerythroblast
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10
Q

What do Reticulocytes tell us about Bone Marrow?

A
  • High RC - BM working well
  • Low RC - BM NOT working well
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11
Q

Importance of EPO

5 functions

A
  1. Stimulate stem cells to differentiate to proerythroblasts
  2. Increase rate of mitosis at each cell maturation stage
  3. Prevent apoptosis of erythroid precursor cells
  4. Increase release of reticulocytes into circulation
  5. Increase Hgb formation
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12
Q

EPO Feedback Loop

A
  1. Kidneys sense low O2-carrying capacity
  2. Secrete more EPO
  3. EPO stimulates erythropoiesis in BM
  4. Increased O2-carrying capacity w/ more RBC
  5. Ends feedback loop
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13
Q

Most common nutritional deficiency in developing and developed countries

A

Iron Deficiency Anemia

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14
Q

Iron deficiency anemia results from 3 things:

A
  1. Decreased iron intake or absorption
  2. Increased iron demans
  3. Increased iron loss
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15
Q

True or False: Nonheme iron is 3 times more absorbable than heme iron

A

False

Heme iron is 3x more absorbable than nonheme iron

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16
Q

Examples of heme iron/ examples of nonheme iron

A

Heme iron: meat, fish, poultry
Nonheme iron: vegetables, fruits, beans, nuts, grain products

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17
Q

Steps of iron absorption

A

Normal diet contains 10-15mg iron in the non-absorbable ferric (Fe3+) state

Stomach acid reduces the iron to the absorbable ferrous (Fe2+) state

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18
Q

Where in the body is ferrous iron primarily absorbed

A

Duodenum and to a lesser extent the jejunum

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19
Q

What % of ingested iron is absorbed?

A

Only 10% BUT deficiency states of increased erythropoiesis can increase absorption to 20-30%

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20
Q

What is ferritin?

A

Iron stores

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21
Q

Example of iron absorption enhancer

A

Vitamin C enhances absorption minimally (200mg of vit C only increases absorption of 30mg og elemnetal iron by about 10%)

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22
Q

Examples of iron absorption inhibitors

A

Tea and coffee consumed in large amounts with a meal (polyphenols can binds iron and decrease non-heme iron absorption)

Calcium (reduces heme and nonheme absorption)

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23
Q

Recommended Daily Iron Intake in…
-Adult males/post-menopausal females
-Menstruating and lactating females
-Pregnancy
-Children

A

-10 mg/day in adult males/post-menopausal females
-15 mg/day in menstruating and lactating females
-30 mg/day in pregnancy
-6-10 mg/day in children (age-dependent)

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24
Q

What are our 2 goals of iron deficiency anemia treatment?

A

1) Replenish iron stores
2) Identify what caused the iron deficiency in the first place

(both equally as important)

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25
Q

True or False: Enteric coated products and slow-release products are recommended for most patients with IDA

A

False

Since an acid medium is required for reduction to the ferrous state and

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26
Q

What is the treatment for IDA?

A

Oral iron

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27
Q

How should we advise patients to take oral iron?

A

Best taken on an empty stomach as food interferes with absorption, but may be impractical due to constipation, N/V/D, stomach upset, other intolerances

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28
Q

Dose for oral iron

A

100-200mg elemental iron per day, usually 1-3 divided doses, for 3-6 months after anemia is resolved

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29
Q

Why do we give oral iron for 3-6 months after anemia is resolved?

A

To build iron stores

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30
Q

What are the 3 traditional iron salts for oral iron treatment?

A

Ferrous sulfate
Ferrous gluconate
Ferrous fumarate

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31
Q

How many oxygens can 1 Hgb hold?

A

4

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32
Q

What is Transferrin?

A
  • transport protein in plasma
  • delivers iron to BM
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33
Q

What are the 3 non-traditional salts for oral iron treatment?

A

Iron polysaccharide complex (also known as feramax)
Heme iron polypeptide (also known as proferin)
Iron bisglycinate

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34
Q

Which iron tablet is the only one connected to heme?

A

Proferin (heme iron polypeptide)

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35
Q

Name some strategies to improve oral iron tolerability

A

-Increase dosing interval
-Switching formualtions with lower amounts of elemental iron
-Start at lower dose, titrate up
-Switch from tablet to liquid, easier titration
-Dietary modificaitons
-Try newer iron formulations
-Can switch to IV iron

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36
Q

What is the Hepcidin response?

A

Our body’s mechanism to control how much iron we absorb from our diet

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37
Q

How does Hepcidin work?

A

It binds to ferroportin leading to degradation of the iron transport channel

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38
Q

What is Ferritin?

A
  • body storage iron
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39
Q

What is Hemosiderin?

A
  • less available storage iron form
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40
Q

RES

A
  • Reticuloendothelial system
  • transferrin delivers extra iron to storage sites: liver, marrow, spleen
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41
Q

Drug interactions with oral iron

A

Levodopa (chelates with iron)
Methyldopa (decreases efficacy of methyldopa)
Levothyroxine (decreases efficacy of levothyroxine)

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42
Q

Oral iron doses (hint include if its ODB or not)

A

Ferrous sulfate 75mg/mL oral liquid (ODB), 300mg tabs

Ferrous gluconate 300mg tabs (ODB)

Ferrous fumarate 300mg caps, 60mg/mL oral liquid (ODB)

Iron polysaccharide complex caps, tabs, liquid powder (not on ODB)

Proferrin tabs (heme iron) (not on ODB)

Iron bisglycinate tabs (not on ODB)

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43
Q

Who is parenteral iron reserved for?

A

Patients who:
-Are unable to tolerate or absorb oral iron
-Inadequate response to oral iron
-Have extensive chronic blood loss or extreme deficit in iron stores who cannot be maintained with oral iron alone
-Need rapid correction of anemia
-Also used in some patients with severe chronic kidney disease (esp if on hemodialysis), some patients with cancer

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44
Q

Name the 4 types of parental iron treatment

A
  1. Iron dextran (infufer, dexiron)
  2. Iron sucrose (venofer)
  3. Sodium ferric gluconate (Ferrlecti)
  4. Iron isomaltoside (Monoferric)
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45
Q

How is Iron dextrain (infufer, dexiron) given?

A

IM - very painful, possible tissue staining
IV - hypersensitivity and anaphylactic reactions possible

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46
Q

How is iron sucrose (venofer) given?

A
  • IV only, less likely to cause hypersensitivity rxs
  • Test dose not required, but consider if the patient has a history of multiple drug allergies
  • Officially indicated for treatment of IDA in CKD patients only
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47
Q

How is sodium ferric gluconate (ferrlecit) given?

A
  • IV only
  • Test dose not required, but consider if the patient has a history of multiple drug allergies
  • Officially indicated for treatment of IDA in hemodialysis patients receiving supplemental EPO
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48
Q

How is iron isomaltoside (monoferric) given?
What is special about it?

A
  • IV only
  • Test dose not required
  • Benefit is that a full dose up to 1500mg or 20mg iron/kg can be given in one session, unlike other available products
  • Officially indicated for any patient with IDA intolerant to oral therapy
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49
Q

True or False: It is recommended that a patient either be on oral iron or IV iron, not both

A

True

No point on being on both oral iron and IV iron at the same time

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50
Q

Why do we need to make sure that parenteral iron is not infused too quickly?

A

Transferrin binding sites can be overloaded, resulting in excess free iron in the bloodstream that can interfere with neutrophil function, perpetuate inflammatory reactions, and compromise active treatment of a coexisting infection

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51
Q

What is a risk of all parenteral iron products?

A

All carry a risk for anaphylactoid reactions and infusion reactions

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52
Q

What is Ganzoni Formula used for?

A

Helps decide how much iron the patient actually needs

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53
Q

What is the Ganzoni Formula?

A

Iron needed (mg) = BW (kg) x target Hb-Actual Hb (g/dL) x 2.4 + iron for iron stores (mg)

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54
Q

3 Types of IV iron reactions

A
  1. Severe/anaphylactoid reactions
  2. Fishbane reactions
  3. Isolated mild/moderate reactions
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55
Q

Severe/anaphylactoid reactions

A
  • <1 in 200,000 doses (super rare)
  • Brochoconstriction, angioedema, trouble breathing, hypotension, severe utricaria, dizziness, fainting, weak pulse, vomiting, abdo pain
56
Q

Fishbane reactions

A
  • 1 in 200 doses
  • Facila flushing, chest tightness, truncal myalgia hallmarks of this reaction
  • No hypotension, no change in SpO2, no edema, no hives or rash
57
Q

Isolated mild/moderate reactions

A
  • IV site irritation
  • Rash/hives
  • Edema
  • Decrease in BP
58
Q

Who is IV iron infusion reserved for?

A

Patients at highest risk
-Hx of infusion reaction
-Asthma
->1 drug allergy

  • If used, typically will include an IV steroid +/- IV H2RA OR IV H1RA
59
Q

IDA adverse effects of treatment for oral, intravenous, and intramuscular

A

Oral:
* Primarily GI (loss of appetite, N/V, constipation, darker stool

Intravenous:
* Immediate hypersensitivity reactions, anaphylaxis is rare
* Fishbane reaction
* Isolated mild/moderate symptoms
* Serum sickness 4-48 hrs after infusion

Intramuscualr
* Soreness and inflammation at injection site and brown skin discoloration

60
Q

Monitoring efficacy and safety for oral iron therapy

A

Efficacy:
* Reticulocytosis within 5-7 days
* Monitor CBC/Ferritin every 1-2 months
* Increase in Hgb of 10g/L every 7-10 days
* Hgb should reach normal by ~2 months
* Ferritin should reach normal by 3-6 months

Safety:
* Ongoing monitoring for GI intolerances

61
Q

Monitoring efficacy and safety for parenteral iron therapy

A

Efficacy:
* Response time for anemia resolution with parenteral is similar to oral, but because IV iron circumvents absorption issues, Hgb/ferritin rise is typically faster

Safety:
* Immedite hypersensitivity reaction monitoring
* Delayed hypersensitivity reaction within 2 days after injection
* Monitor monthly: ferritin, TSAT to assess for overload
* Symptoms of iron overload, LFTs if signs/sx of overdose

62
Q

B12 Deficiency Anemia: who has a decreased intake rare

A

-Strict vegans and their breastfed infants
-Chronic alcoholics
-Elderly patients with severely restrictive diet

63
Q

B12 Deficiency Anemia: who has decreased absorption

A

-Occurs with intrinsic factor deficiency (pernicious anemia)
-Atrophy of gastric mucosa
-Stomach surgery
-PPi/H2RA
-Metformin
-Ileal resection
-Crohn’s disease
-Chronic pancreatitis
-Blind loop syndrome
-Whipple disease
-Zollinger-Ellison syndrome

64
Q

How we absorb cobalamin (vitamin B12)

A
  1. Intake of dietary cobalamin bound to animal protein
  2. Gastric secretion of HCl and pepsin releases cobalamin from protein
  3. Low pH favors cobalamin binding to haptocorrins
  4. Pancreatic protease degrades haptocorrin
  5. Increased pH favours cobalamin binding to intrinsic factor
  6. Cobalamin-intrinsic factor complex binds to cubam receptor on ileal mucusal cells and is internalized
65
Q

Explain the decreased utilization in B12 deficiency anemia

A

Vitamin B12 is bound to a transport protein called transcobalamin II that moves it around the blood to areas of need and storage. In patients with deficiencies in this, this process is inhibited

66
Q

Goals of B12 deficiency anemia treatment

A
  1. Aim is to replenish B12 stores, normalize HgB
  2. Identify what caused the B12 deficiency in the first place
67
Q

True or False: Patients can replenish their vitamin B12 deficiency by simpling eating more meat

A

False

It is difficult to get enough vitamin B12 to treat this anemia just from

68
Q

Parenteral treatment for B12 deficiency anemia

A

IM cyanocobalamin
-Cyanocobalamin is the synthetic form of B12
-1000 micrograms IM daily for 1-2 weeks to saturate B12 stores, followed by 100-1000 micrograms per week until clinical manifestatons resolve
-Then monthly injections of 100-1000 micrograms until cause is resolved

69
Q

B12 Deficiency Anemia Oral treatment

A
  • Lower dose oral B12 + oral intrinsic factor
  • higher dose oral B12 alone (1000-2000 mcg/day)
70
Q

B12 Deficiency Anemia: Oral vs Parenteral

A
  • If a patient has severe symptomatic anemia and/or neurological complications, IM route generally preferred as initial therapy
  • If reduced dietary intake: PO route
  • If altered GI anatomy: parenteral
  • If impaired absorption: both are equivalent
71
Q

B12 Deficiency Anemia: Intranasal Treatment

A
  • In US, not in Canada
  • 500 mcg/0.1mL
  • More bioavailable than oral route
  • if used, suggest reserve for maintenance therapy after hemotologic parameters have normalized
72
Q

B12 deficiency anemia monitoring for efficacy and safety

A

Efficacy:
-Patients will start feeling better in a few days
-Bone marrow becomes normoblastic within 24 hours
-Reticulocytosis within 3-5 days
-Check CBC and serum vit B12 levels in 1-2 months
-Neurological function can improve within 24-48 hours but complications can take months-years to resolve

Safety:
-Well tolerated, monitor injection site for IM and GI upset for PO
-Uncommon side effects: headache, weakness, and hypokalemia
-Elevated vit B12 plasma levels associated with increased risk of cancer and mortality (causation not proven)

73
Q

Who is at risk of folic acid deficiency anemia decreased intake?

A

-Elderly patients
-Teenagers and “junk food” diets
-Alcoholics (caloric intake from alcohol)
-Chronically ill or patients with dementia
-Low income

74
Q

Who is at risk of folic acid deficiency anemia decreased absorption?

A

-Malabsorption syndromes
-Alcoholism
-Tropical sprue
-Celiac disease
-Crohns disease
-Certain medications

75
Q

Drugs that induce folate deficiency

A

-Anticonvulsants (phenytoin, primidone, phenobarbital)
-Folate antagonists (methotrexate, pentamidine, trimethoprim, triamterene)
-Oral contraceptives
-Alcohol
-Sulfasalazine
-Direct inhibitors of DNA synthesis (azathioprine, hydroxyurea, zidovudine, 6-mercaptopurine)

76
Q

Where do we see folic acid deficiency anemia hyper-utilization (where rate of cellular division is increased)

A

-Pregnancy
-Myelofibrosis
-Malignancy
-Infants and adolescents at growth spurts
-Chronic inflammatory conditions
-Hemolytic anemia

77
Q

Goals of treatment for folic acid deficiency anemia

A
  1. Aim to replenish folate stores
  2. Identify what caused the folate deficiency in the first place
78
Q

Oral folate for folic acid deficiency anemia

A

-1-5 mg/day orally
-Treatment for 4 months to allow for clearance of folate deficient RBCs from the circulation, but lifetime administratio may be necessary
-Folate will partially correct the RBC changes of pernicious anemia, but will not prevent the neurosensory changes

79
Q

Monitoring for efficacy and safety of folic acid deficiency anemia

A

Efficacy:
-Increased alertness and appetite occur early in treatment course
-Reticulocytosis begins within 3-5 days
-MCV initially increased due to increased reticulocytosis, but gradually decreases to normal
-Check CBC and serum folic acid in 1-2 months

Safety:
-Folic acid generally very well tolerated

80
Q

What is associated with anemia of chronic disease?

A

-Decreased RBC survival
-Blunted EPO activity in bone marrow
-Impaired proliferation of erythroid progenitor cells
-Relative EPO deficiency
-Decreased utilization of reticuloendothelial iron for hemoglobin synthesis
-Various disturbances in iron homeostasis

81
Q

Treatment goals for anemia of chronic disease

A

-Treat the underlying condition
-Iron supplementation if iron deficiency present
-Erythropoiesis-stimulating agent (ESA)

82
Q

What is hemolytic anemia?

A

-Decreased survivial time of RBCs due to destruction in spleen or in circulation
-Can be mild, chronic, acute, severe or life-threatening

83
Q

What is the RBC lifespan for hemolytic anemia?

A

120 days

84
Q

2 causes of hemolytic anemia

A
  1. Intrinsic (intracorpuscular changes of RBCs)
  2. Extrinsic (extracorpuscular changes of RBCs)
85
Q

What causes intrinsic hemolytic anemia?

A

Sickle cell anemia
-Inherited condition, RBC lifespan 10-20 days
-Amino acid substitution in the B-chain of Hgb causes sickling of deoxygenated Hgb

86
Q

3 types of crisis’ in sickle cell anemia

A
  1. Vaso-occlusive pain crisis
  2. Aplastic crisis
  3. Acute splenic sequestration crisis
87
Q

What is vaso-occlusive pain crisis

A

-Sticky sickled cells block blood vessels to lungs, abdomen, joints, bones, spleen, liver
-Pain develops in those regions (can last hours to weeks)
-Sickled cells also block blood flow to hands and feet, causing them to swell (hand-and-foot syndrome)

88
Q

What is aplastic crisis?

A

-Rapid decline in Hgb and decrease reticulocytes
-Hypoplastic bone marrow usually due to bacterial or viral infection
-Headache, fatigue, tachycardia, dyspnea

89
Q

What is acute splenic sequestration crisis?

A

-Sudden enlargement of spleen, sequestering RBCs from reticuloendothelial system
-HCT, Hgb fall dramatically
-Drop in blood volume = hypotension and shock

90
Q

Sickle cell anemia treatment

A

-Hydroxyurea can reduce vaso-occlusive pain crises, increase survival, and improve QOL
-Hydroxyurea used to increase fetal Hgb production which help maintain rounder shape and deformability of RBCs
-Patients often require frequent transfusion and symptomatic management

91
Q

What is glucose-6-phosphate dehydrogenase deficiency

A

-Inherited condition x-linked
-G6PD reduces NADP to NADPH, which maintains glutathione in the reduced state
-Without reduced glutathione, hemoglobin is oxidized and denatured (Heinz bodies)
-Heinz bodies damage the cell membrane and are removed by the spleen

92
Q

What are triggers of glucose-6-phosphate dehydrogenase deficiency?

A

-Infections
-Certain medications (primaquine, nitrofurantoin)
-Certain foods (fava beans, bitter melon)
-Mothballs
-Henna

93
Q

True or false: most glucose-6-phosphate dehydrogenase deficiency is asymptomatic

A

True

Also male > female in symptomatic presentation

94
Q

What is the treatment for glucose-6-phosphate dehydrogenase deficiency?

A

Blood transfusions

95
Q

Hemoglobin releases O2 when…

A
  • increased [CO2]
  • increased [H+] (decreased pH)
  • increased temp
  • increased 2,3-diphosphoglycerate (2,3-DPG)
96
Q

What does Increased 2,3-DPG cause?

A
  • causes decreased Hgb affinity for oxygen
97
Q

Macrocytic Anemia

morphology

A
  • RBC > 100 fL
  • Vit B12 deficiency, Folic acid deficiency, (nonmegaloblastic - more RC circulating)
98
Q

Microcytic, hypochromic Anemia

morphology

A
  • RBC < 80 fL
  • iron deficiency, sickle cell anemia, thalassemia, chronic disease
99
Q

Normocytic Anemia

morphology

A
  • RBC 80-100 fL
  • blood loss, hemolysis, BM failure, renal failure, endocrine disorders, myelodysplastic, chronic disease
100
Q

Normochromic Anemia

morphology

A
  • RBCs have normal colour
  • ex. Acute blood loss, EPO deficiency
101
Q

Hypochromic Anemia

morphology

A
  • RBCs paler than normal
  • ex. Iron deficiency, chronic disease, thalassemia
102
Q

Examples of Anemia caused by Deficiency

Etiology

A
  • iron, B12, folic acid, pyridoxine
103
Q

Examples of Anemia caused by Central (marrow) causes

Etiology

A
  • chronic disease, elderly, malignancy
104
Q

Examples of Anemia caused by Peripheral causes

Etiology

A
  • hemorrhage, hemolysis
105
Q

Blood Loss Anemia

Pathophysiology

A
  • acute, chronic
106
Q

Hemolytic Anemia

Pathophysiology

A
  • inherited, acquired
107
Q

Impaired Production Anemia

Pathophysiology

A
  • chronic disease, aplastic anemia, iron deficiency, folate deficiency, sideroblastic
108
Q

Hemoglobinopathy

Pathophysiology

A
  • sickle cell, thalassemia
109
Q

What does a Decreased Reticulocyte Index mean?

A
  • anemia due to impaired BM, iron/B12 deficiency, chronic disease, malnutrition, renal
110
Q

What does an increase in Reticulocyte Index mean?

A
  • cause unrelated to BM, acute blood loss, hemolysis
111
Q

What does a decreased Serum Iron mean?

A
  • infection/inflammation, chronic anemia, IDA
112
Q

What does an increased Serum Iron mean?

A
  • hemolytic anemia, iron overload (hemochromoatosis)
113
Q

Transferrin is a ____ phase protein

A
  • negative acute phase protein
  • meaning it production of Transferrin decreases under a state of inflammation, trauma or infection
114
Q

Increased TIBC means…

A
  • iron stores are low (more binding sites)
  • increased TIBC + low serum iron suggests IDA
  • oral contraceptive use/pregnancy
115
Q

Decreased TIBC means…

A
  • decreased amount of transferrin (infection, inflammation, liver disease, uremia)
116
Q

What does TSAT <15% mean

A
  • Iron Deficient Anemia
117
Q

Ferritin is a ____ phase protein

A
  • positive acute phase protein
  • meaning it increases under a state of inflammation, trauma, infection
118
Q

Decreased Serum Ferritin means…

A
  • iron deficiency b/c ferritin decreases when there are truly low body iron stores
  • <15 ug/L -> iron deficiency
119
Q

Increased Serum Ferritin means…

A
  • high body storage of iron OR chronic infection/inflammation
120
Q

Decreased Folic Acid levels means…

A
  • folate deficiency anemia, may co-exit w/ B12 deficiency anemia
121
Q

____ is more useful to assess folate deficiency

A
  • Serum Folate
122
Q

What might mask a Vitamin B12 Deficiency?

A
  • Treating a folic acid deficiency may mask a B12 deficieny by normalizing Hgb levels
123
Q

Decrease Vitamin B12 (cobalamin) levels means…

A
  • indicates vit B12 deficiency, may co-exist w/ folate deficiency
124
Q

Steps in absorbing Vitamin B12

A
  1. Cobalamin bound to animal protein
  2. Gastric secretion of HCl & pepsin releases Cbl from protein
  3. Low pH in stomach favours Cbl binding haptocorrin
  4. Pancreatic protease degrades haptocorrin
  5. High pH favours Cbl binding IF
125
Q

What does Schilling’s Urinary Excretion Test Diagnose?

A
  • Diagnose B12 deficiency caused by a lack of intrinsic factor which facilitates ileal absorption of B12
126
Q

Stages of Schilling’s Urinary Excretion Test

A
  1. Oral dose of radio-labeled B12 + large dose (1000mg IM) of non-labeled B12 1 hr later to saturate tissue binding sites
  2. If normal amt of labeled B12 is found in urine, IF deficiency is confirmed, if test is low go to step 3
  3. Tetracycline 250mg QID x 10d + radio-labeled B12 - improves then bacterial overgrowth interfering w/ B12 absorption
  4. Pancreatic enzymes x 3d + radio-labeled B12 - improves indicates malabsorption due to pancreatic insufficiency
127
Q

Increased Homocysteine means…

A
  • B12 & folate deficiency
128
Q

Increased Methylmalonic Acid (MMA)…

A
  • B12 deficiency
129
Q

What does Coombs Test measure? Direct vs. Indirect.

A
  • Anti-globulin test indicating hemolytic anemia caused by autoimmune response
  • Direct – detects self-attacking Abs bound to RBCs, +ve indicates autoimmune mediated hemolysis
  • Indirect – measures Abs in serum
129
Q

Symptoms common to ALL Anemias

A
  • Fatigue
  • Pallor
  • Tachycardia
  • Wide pulse pressure
  • Pale mucous membranes
  • SOB
  • Edema
  • Cardiac decompensation (high output CHF)
  • Dizziness
130
Q

Iron Deficiency Anemia Symptoms

A
  • Koilonychia (spooning of nails)
  • Angular stomatitis (angular cheilitis)
  • Strophic glossitis (inflam. of tongue)
  • Achlorhydria (no HCl in gastric secretions)
  • Pica (craving clay, ice, cornstarch)
  • Restless leg syndrome
131
Q

Vitamin B12 Deficiency Anemia Symptoms

A
  • Dysphagia
  • Weight loss
  • Beefy red tongue
  • Psychosis
  • Forgetfulness
  • Paresthesia of hands & toes
  • Ataxia
  • Impaired vibratory sense
  • Impaired position sense
  • Romberg sign
  • Babinski reflex
  • Impaired urinary function
132
Q

Folic Acid Deficiency Anemia Symptoms

A
  • Dysphagia
  • Beefy red tongue
  • Personality changes
  • Anorexia
  • Weight loss
  • Generalized malnutrition
  • Ecchymosis (bruising)
  • Purpura
  • Loss of skin elasticity
  • Early graying of the hair
133
Q

Hemolytic Anemia Symptoms

A
  • Painful crisis
  • Abdominal pain
  • Hemoglobinuria
  • Cholelithiasis
  • Leg ulcers
  • Fever (rare)
  • Jaundice (rare)
  • Lymphadenopathy (rare)
  • Angina (rare)
  • Syncope (rare) – fainting
  • Heart failure (rare)
134
Q

Chronic Disease Anemia Symptoms

A
  • Depends more on nature of underlying disease
  • Anemia usually mild to moderate
  • Infection
  • Inflammation
  • Malignancy w/ BM disorders

PHARM 220 (4 decks)

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