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Year 3 - Clinical > 28 - Anemia > Flashcards

28 - Anemia Flashcards

1
Q

What is anemia?

A
  • Group of diseases characterized by decrease in either hemoglobin or volume of RBCs which results in decreased oxygen-carrying capacity of the blood
  • Sign of underlying pathology rather than a disease
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2
Q

How is anemia characterized?

A
  • Can be characterized by RBC size (macrocytic, normocytic, or microcytic)
    • Vitamin B12 & folate deficiencies are both macrocytic anemias
    • Microcytic = iron deficiency
    • Normocytic = recent blood loss or chronic disease
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3
Q

Main causes of anemia

A
  • Inadequate RBC production
  • Ineffective RBC maturation (iron deficiency, vitamin B12 & folic acid deficiency)
  • Increased RBC destruction
  • Increased RBC loss
  • More than 1 anemia & etiology can occur at the same time
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4
Q

Describe the assessment for anemia

A
  • 5 steps -> See How Many Red Cells (SHMRC)
    • S = signs & sx (look for first)
    • H = hemoglobin or hematocrit (if low = anemic)
    • M = MCV (indication of average RBC size)
    • R = RDW (or peripheral blood smear) – are all cells the same size? Do you believe the MCV? – normal RDW = 11-14%
  • – If MCV is normocytic, might assume that RBC’s are normal w/o anemia
  • – If RDW is high, means big difference between size of RBC’s => anemia
  • – Iron deficiency anemia produces microcytic MCV, but may start off as normal & RDW will be high (above normal) b/c don’t have all the same size RBCs
    • C = check reticulocytes & likely deficiencies
  • – Reticulocytes = immature RBC’s released from bone marrow
  • Be aware of mixed anemias
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5
Q

General clinical presentation of anemia

A
  • CNS = fatigue, headache, dizziness
  • HEENT (head, eyes, ears, nose, throat) = pale skin, conjunctivae, & nail beds; vertigo
  • Respiratory = dyspnea on exertion
  • CVS = tachycardia, palpitations
  • GI = anorexia
  • Other = cold intolerance, loss of skin tone
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6
Q

What labs are used to assess anemia?

A
  • CBC (Hbg, Hct including RBC indices – MCV, MCHC, RDW)
  • Iron indices (ferritin), vitamin B12, folate
  • Reticulocyte index
  • Stool sample for occult blood
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7
Q

Lab definition of anemia

A
  • Males = Hgb < 130 g/L

- Females = Hbg < 120 g/L

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8
Q

What do the values of MCV and RDW mean in regards to anemia?

A
  • Microcytic (MCV < 80 fL)
    • Normal RDW = ACD (anemia of chronic disease)
    • High RDW = iron deficiency (ferritin < 20 mcg/L)
  • *Don’t use RDW to differentiate between IDA & ACD
  • Normocytic (MCV 80-100 fL)
    • Normal RDW = CKD; ACD; hypothyroidism
    • High RDW = hemolytic anemia; sickle cell anemia
  • *Check reticulocytes
  • Macrocytic (MCV > 100 fL)
    • Normal RDW = liver disease; EtOH
    • High RDW = B12/folate deficiency
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9
Q

What is the most common cause of anemia?

A

Iron deficiency

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10
Q

Presentation of iron deficiency anemia

A
  • Clinical presentation = dry rough skin, brittle nails, dry damaged hair or hair loss, restless leg syndrome (b/c epithelial cells that rapidly divide need iron, so w/ iron deficiency they can’t divide as quickly & will dry up)
  • Signs of advanced tissue iron deficiency = cheilosis (cracking at corners of mouth) & koilonychia (spooning of fingernails)
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11
Q

Describe how to determine severity of anemia sx

A
  • Mild = little to no sx
  • Moderate = sx affecting life; fatigue, weakness, difficulty concentrating
  • Severe = unable to tolerate mild exercise, may be symptomatic at rest
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12
Q

Describe the lab values measured in regards to iron

A
  • Serum ferritin (20-300 mcg/L)
    • Reflects tissue iron stores (liver, spleen, bone marrow)
    • Acute phase reactant (may be elevated in infection, inflammation, malignancy)
    • If ferritin is low (< 20) probably deficient in iron
    • If ferritin high (> 100) likely have a chronic disease & must check TSAT
  • TSAT (%) = serum iron/TIBC * 100%
    • Amount of iron readily available (how much iron is in blood & available to bone marrow to make new RBCs)
    • Normal = 14-50%
    • Usually only measured if ferritin is normal (or in CKD)
    • Basically, saying how much transferrin is bound to iron in the blood
    • TIBC total iron binding capacity (47-72 umol/L) – indirect measure of iron-binding capacity of serum transferrin
    • Serum iron (7-27 umol/L) – concentration of iron bound to transferrin
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13
Q

What are the lab findings of iron deficiency anemia?

A
  • Hgb = low
  • MCV = low (microcytic)
  • MCH = low (microcytosis or hypochromia)
  • MCHC = low (hypochromic = less pigment, so pale)
    • Normochromic or hypochromic = Hgb content
    • Independent of cell size, so more useful than MCH in distinguishing between microcytosis & hypochromia
    • Low MCHC = hypochromia (microcyte w/ normal hemoglobin concentration will have low MCH but normal MCHC); most often seen in iron-deficiency anemia
  • RDW = high (variation in size of RBCs)
  • Reticulocytes = low-normal (impaired RBC production)
  • Serum ferritin = low (< 20 mcg/L)
    • Serum ferritin is proportional to total iron stores, so is the best indicator of iron deficiency or iron overload
    • Low serum ferritin is basically diagnostic of IDA
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14
Q

What is MCH and what is the most common cause of elevated MCH?

A
  • Amount of hemoglobin in an RBC & usually increases or decreases w/ the MCV
  • Most common cause of elevated MCH is macrocytosis (vit B12 or folate deficiency)
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15
Q

What is MCHC?

A

Concentration of hemoglobin per volume of cells

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16
Q

Risk factors for IDA

A
  • Inadequate intake/increased requirements
    • Adolescents (poor diet, rapid growth)
    • Menorrhagia, pregnancy/lactation
    • Vegetarians (especially vegans)
    • Athletes (increased RBC production, iron loss, sweat)
    • Chronic renal failure px
  • Blood loss – regular blood donors, surgery, drugs (NSAIDs, ASA, anticoagulants; antacids can decrease iron absorption)
  • Genetic – family history of hematologic disorders; ethnicity
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17
Q

Goals of tx for IDA

A
  • Improve clinical signs & sx of anemia

- Restore Hgb levels & MCV to normal & replenish iron stores

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18
Q

Principles of tx for IDA

A
  • Determine cause of iron deficiency & treat underlying disease if possible
    • Fecal occult blood test (FOBT) to check for GI bleeding/colon cancer screening
  • Replenish iron stores
    • Options = increase dietary iron (very hard to get rid of deficiency w/ just dietary intake), oral iron supplementation, IV iron supplementation, blood transfusions
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19
Q

Causes of IDA

A
  • Increased iron loss (ex: menses, GI neoplasms, blood donation, peptic ulcer, hemorrhoids, drugs like ASA, NSAIDs, anticoagulants)
  • Increased demand for iron (ex: rapid growth in infancy/adolescence, pregnancy, EPO deficiency)
  • Decreased iron intake/absorption (ex: inadequate diet, gastric surgery, Crohn’s disease, celiac disease, achlorhydria/low gastric acid, acute or chronic inflammation, H. pylori infection)
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20
Q

What is the difference between heme iron and non-heme iron and what are sources of each?

A
  • Heme iron Fe2+ (ferrous iron)
    • Meat, poultry, seafood
    • 3x more absorbable vs. non-heme iron (has different receptor that it binds to in gut & less things block its absorption)
    • Absorption decreased by content of calcium in meal (Ca2+ supplements, milk/dairy)
  • Non-heme iron Fe3+ (ferric iron)
    • Vegetables, fruits, dried beans, nuts, grains
    • Absorption increased by gastric acid & ascorbic acid-rich foods
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21
Q

What decreases non-heme iron absorption?

A
  • Phytates (bran, oats, rye fiber)
  • Tannins (herbal teas) – don’t recommend tea if trying to keep iron levels up
  • Phosphates
  • Polyphenols (tea/coffee)
  • Calcium supplements
  • Milk/dairy
  • Antacids, PPIs, H2 blockers
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22
Q

Recommended dose of oral iron for IDA? How should it be taken?

A
  • Recommended dose for IDA = 150-200 mg elemental Fe/day (or 2-3 mg/kg/day)
    • Elderly = 15-50 mg/day may be effective (especially if mild deficiency)
  • Take on empty stomach or at least 1 h before meal or 2 h after meal
  • May need to take w/ meals to decrease GI side effects (decreases absorption)
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23
Q

SE and drug interactions of oral iron?

A
  • SE = N/V, dyspepsia, constipation, diarrhea, dark stools (remember to warn px)
    • Generally, dose related & resolve w/ time
    • Start w/ 1 tab and work up gradually to improve GI tolerability
  • Drug interactions = antacids, PPIs, H2 blockers, calcium/milk, levodopa, levothyroxine, quinolones, tetracyclines, bisphosphonates
  • Consider holding iron until antibiotics completed (iron is a growth factor for bacteria & don’t want antibiotic to not be absorbed, so easiest to hold iron)
  • For px w/ CKD, often are on calcium at meals as a phosphate binder, so give iron 3 tabs HS b/c better absorbed on empty stomach
24
Q

Which oral iron preparation should you choose? know this

A
  • Various iron salts contain different amounts of iron (all absorbed similarly)
  • SR formulations not good b/c release past duodenum may decrease chance for absorption
  • Enteric coated more poorly absorbed than standard film-coated (b/c iron needs to be exposed to acid to be absorbed)
  • Ferrous gluconate (11% Fe, 35 mg/300 mg tab), sulphate (20% Fe, 60 mg/300 mg tab), & fumarate (33% Fe, 100 mg/300 mg tab)
    • Rarely start someone who’s never had iron supplement w/ fumarate
    • Generally, start on 1 sulfate & titrate up to 3 tabs
    • If someone says they used iron supplements & had horrible side effects, start w/ 1 gluconate & slowly titrate up
25
Q

When should parenteral iron be considered? What is a disadvantage to this type of iron?

A
  • Evidence of iron malabsorption, intolerance to oral iron, pt w/ significant blood loss who refuses blood transfusion & can’t take oral iron, chronic dialysis px, some px receiving chemotherapy & erythropoiesis stimulating agents (ESAs)
  • All parenteral iron preparations carry a risk for anaphylactic reactions
26
Q

How is IV iron dose calculated?

A
  • For iron deficiency anemia (adults) not px requiring iron replacement for blood loss
  • Dose of iron (mg) = weight (kg) * (140 – Hgb) * 0.22
    • “Desired Hbg” can adjust to 120 or 130
  • Additional quantity of iron to replenish stores should be added (~600 mg for women & 1,000 mg for men)
  • Usually given in divided doses
  • *Don’t give w/ oral iron as GI absorption would be impaired
27
Q

Possible adverse reactions w/ IV iron

A
  • Transient side effects (usually resolve w/in 48 h) = N/V, pruritus, headache, flushing, myalgia, back & chest pain
  • Hypersensitivity reactions (rare)
  • Severe or life-threatening reactions (rare) – risk factors = rapid infusions, history of atopy & drug allergy
  • Px are monitored closely during administration
28
Q

Describe the use of blood transfusions for anemia

A
  • Indicated if acute blood loss w/ hemodynamic compromise
  • 1 mL packed RBCs ~ 1 mg iron (ex: 2 units of PRBCs = 500 mL = 500 mg iron)
  • 1-unit PRBC increases Hgb by ~ 10 g/L
  • Concerns = safety, availability
  • Considered for those w/ severe anemia (Hgb < 70-80 g/L)
29
Q

What is monitored w/ IDA?

A
  • Therapeutic doses of iron should increase Hgb by 10 g/L per week (response of < 20 g/L over 3 weeks = further evaluation needed)
  • CBC (Hgb) q1month x 3-6 months (increase of Hgb by 2 weeks, normalization of Hgb by 6-8 weeks)
  • Ferritin, +/- TSAT in 3-6 months
  • Treat for 3-6 months after anemia resolved to allow for repletion of iron stores & prevent relapse (~6-12 months)
  • Important to monitor for SE & sx improvement
30
Q

Describe vitamin B12 deficiency anemia

A
  • IF (intrinsic factor) = main receptor for vit B12 to be absorbed (some people lack IF b/c formed antibodies against & destroy it) => pernicious anemia is type of vitamin B12 deficiency
  • MMA = methylmalonic acid & homocysteine tests can determine this anemia
    • These are expensive tests & rarely used; only used if B12 levels are borderline & need more info
  • Conversion of MMA to succinyl-CoA requires B12 & conversion of homocysteine to methionine requires vitamin B12 and folate
  • *Know that major sx difference between folate & B12 deficiency = neurologic sx (tingling, numbness, dementia, ataxia) only in B12 deficiencies b/c B12 required to produce myelin for neurons
  • Role of vitamin B12 (cobalamin) – required w/ folic acid in synthesis of DNA & RNA, essential for maintaining integrity of neurologic system, role in fatty acid synthesis & energy production
31
Q

What are some dietary sources of vitamin B12?

A
  • Meat, fish, poultry
  • Dairy
  • Fortified cereals
32
Q

How long does vitamin B12 deficiency take to develop? Why?

A
  • Several years (5-10 years)

- Due to efficient enterohepatic circulation & body stores (hence why more common in elderly)

33
Q

What are the lab findings in vitamin B12 deficiency?

A
  • Hgb = low
  • MCV = high (macrocytic)
    • MCV changes can precede low B12 levels by months
  • Serum B12 = low
    • Vit B12 levels may be falsely low w/ folate deficiency
  • Homocysteine = high
  • MMA = high
  • WBC, platelets = low (mild)
  • Reticulocytes = low (want it to be high)
34
Q

Signs and sx of vitamin B12 deficiency anemia

A
  • In addition to general sx of anemia
  • Neurologic = early (numbness, paresthesia’s) or later (peripheral neuropathy, ataxia, imbalance)
    • If elderly px has unexplained/acute dementia or neuropathy, must rule out vitamin B12 deficiency b/c if not treated will be irreversible
  • Muscle weakness
  • Irritability, personality changes, memory impairment
35
Q

Causes of vitamin B12 deficiency

A
  • Inadequate intake (rare) – strict vegans, chronic EtOH, elderly diet (tea & toast)
  • Malabsorption – pernicious anemia (no intrinsic factor), cobalamin malabsorption (inadequate gastric acid production; needed for cleavage of vit B12 from proteins in diet), Rx acid suppression
  • Inadequate utilization (uncommon) – lack of transport protein
36
Q

Pernicious anemia - what is it? Causes? Risk factors?

A
  • Absence of intrinsic factor
  • Anti-intrinsic factor antibodies – positive in 50%
  • Causes = autoimmune destruction of gastric parietal cells, atrophy of gastric mucosa, stomach surgery
  • Risk factors = age (increases over age 60), women > men
37
Q

What can cause drug-induced megaloblastic anemia?

A
  • Direct inhibitors of DNA synthesis (azathioprine, hydroxyurea, chemotherapy)
  • Folate antagonists (carbamazepine, phenytoin, valproic acid, methotrexate, trimethoprim)
  • Reduced folate/vitamin B12 absorption (excessive EtOH, ASA, colchicine, metformin, oral contraceptives)
38
Q

Tx of vitamin B12 deficiency anemia

A
  • Subcut/IM vitamin B12 (cyanocobalamin) *start this when pt experiencing neurologic sx
    • 800-1000 mcg daily for 1-2 weeks to saturate stores, then
    • 100-1000 mcg weekly until Hgb/Hct normal, then
    • 100-1000 mcg monthly to maintain normal erythrocyte count
  • Oral vitamin B12 (cyanocobalamin or methylcobalamin) 1000-2000 mcg daily
  • Treat early to reduce risk of irreversible neurologic damage
  • Life time therapy if underlying cause not corrected
39
Q

How to decide IM vs. oral vitamin B12

A
  • Daily PO (1000-2000 mcg) vit B12 as effective as IM for hematologic/neurologic response even in pernicious anemia
  • IM/subcut recommended for:
    • Neurologic sx, until resolved, then may switch to PO
    • Hospitalized px
    • Poor GI absorption
    • Unable to take PO
    • Diarrhea/vomiting
    • Noncompliance
40
Q

Monitoring for vitamin B12 deficiency anemia

A
  • Reticulocytosis in 3-5 days (peaks at 7 days)
  • Hematologic improvement (Hgb, WBC) in 5-7 days
  • MMA, homocysteine decreases start at 1-2 weeks
  • Vitamin B12 deficiency resolves in 3-4 weeks (improved strength & well-being w/in a few days)
  • 6 months or longer required for improvement of neurologic signs/sx
  • Check CBC & vitamin B12 levels at 1-2 months, then at 3-6 mo
  • Check homocysteine & MMA at 2-3 months
41
Q

Describe folic acid deficiency anemia

A
  • Role of folic acid = production of DNA & RNA, necessary to form methylcobalamin which converts homocysteine to methionine
  • Humans unable to synthesize sufficient folate, so dietary sources needed
42
Q

Dietary sources of folic acid

A
  • Fresh green leafy vegetables
  • Citrus fruits
  • Mushrooms
  • Dairy products
  • *Cooking > 15 min in lots of water destroys high proportion of folate
43
Q

How much folate does the body store and where?

A

~5-20 mg in the liver

44
Q

Causes of folic acid deficiency anemia

A
  • Inadequate intake – elderly, alcoholics, poverty, chronic illness/dementia, teenager (junk food diet)
  • Decreased absorption – Crohn’s disease, celiac disease, alcoholism, drugs
  • Hyperutilization (increased requirement) – pregnancy, hemolytic anemia, malignancy, chronic dialysis
  • Altered metabolism – drugs (folate antagonists, DNA synthesis inhibitors)
45
Q

Folic acid deficiency anemia – lab findings

A
  • Hgb = low
  • MCV = high (macrocytic)
  • RBC = low
  • Serum folate not tested in WPG b/c very inaccurate
  • Homocysteine = high
  • MMA = normal
  • Vitamin B12 = normal
  • *Must rule out vitamin B12 deficiency!!! Can’t treat folate deficiency w/o making sure they don’t have vit B12 deficiency
46
Q

Folic acid deficiency anemia – tx

A
  • Oral folic acid (folate) – 1 mg daily, 5 mg daily if absorption compromised (ex: EtOH)
  • Tx continued until cause of deficiency identified & corrected
  • 4 months therapy in order for folate-deficiency RBCs to be cleared (life span of RBC)
47
Q

Monitoring for folic acid deficiency anemia

A
  • Sx improvement (increased alertness & appetite) occurs early
  • Reticulocytosis in 2-3 days (peaks at 5-8 days)
  • Hgb, Hct increases w/in 2 weeks, normalizes in 2 months
  • Measure CBC at 1 mo then at 3-6 mo; RBC folate at 4 mo; homocysteine & MMA at 2-3 mo
48
Q

Describe anemia of chronic disease (ACD). Common causes and goal of tx?

A
  • AKA anemia of inflammation
  • Most common normocytic anemia (also can be microcytic)
  • Usually diagnosis of exclusion (nonspecific sx, important to rule out iron deficiency & blood loss)
  • Common causes = chronic infection (HIV, UTIs, osteomyelitis), malignancy, chronic inflammation, CKD
  • Generally, develops after 1-2 months of sustained disease
  • Goal (if possible) treat underlying cause
49
Q

ACD – lab findings

A
  • Hgb = mild (> 95 g/L) to moderate (> 80 g/L) – usually ~100-110 g/L
  • MCV = normal or low
  • RDW = normal
  • Reticulocytes = low (b/c inflammatory mediators are suppressing bone marrow so not producing as many RBCs)
  • TIBC (transferrin) – normal or low in ACD; high in IDA
50
Q

Describe when to initiate ESA

A
  • If Hgb < 100 g/L, individualize based on:
    • Rate of fall of Hgb
    • Prior response to iron therapy
    • Risk of needing a transfusion
    • Risks related to ESA therapy
    • Anemia sx
  • Don’t maintain Hgb > 115 g/L
  • Don’t intentionally increase Hgb > 130 g/L
  • Caution w/ ESA use for active malignancy, recent stroke, hx of cancer
51
Q

Describe the iron targets in CKD

A
  • All CKD px on ESAs should have adequate iron stores before initiation/increasing dose of ESA
  • For any pt on ESA, if not on iron should be put on iron
    • If no dialysis – try oral iron
    • If on hemodialysis – use IV iron b/c probably won’t absorb oral
52
Q

Treatment of ACD

A
  • Iron supplementation – required by most px receiving ESAs due to increased iron demand resulting from stimulation in RBC production
  • ESAs – consider when Hgb 90-100 g/L
  • Vitamin B12 & folate supplementation – vitamins B, C, & folic acid (water-soluble vitamins) often depleted w/ renal diet & hemodialysis therapy
53
Q

Erythropoiesis-stimulating agents (ESAs) available products and dosing

A
  • Epoetin alfa (Eprex) – given subcut or IV 1-3 times/week
  • Darbepoetin alfa (Aranesp) – subcut or IV q1-2weeks
  • ESA dosage adjustments – usually 25% dosage increments; pay attention to Hgb trends
54
Q

Describe ESA resistance

A
  • Iron deficiency (main cause)/folic acid or B12 deficiency

- Underlying infection, inflammatory condition, or malignancy

55
Q

What are some warnings w/ ESAs?

A
  • High targets (> 120 g/L) associated w/ strokes, thromboembolic events, CV events, & possible increased risk of cancer
  • Original Hgb targets were 110-120 g/L
  • Don’t initiate unless Hgb < 100 g/L & use lowest ESA dose necessary to decrease need for RBC transfusions
56
Q

What are the available IV iron products? When should they not be used?

A
  • Dextran, sucrose (Venofer), & sodium ferric gluconate complex (Ferrlecit) are the available products
  • Avoid giving IV iron to px w/ active systemic infections
57
Q

Monitoring anemia in CKD

A
  • CBC every month – acceptable rate of Hgb rise ~ 10-20 g/L per month
    • Don’t increase dose more often than q4weeks
    • Decrease dose by 25% if Hgb increases > 10 g/L in 2 weeks
    • Increased dose by 25% if Hgb increases < 10 g/L in 4 weeks (rule out ESA resistance)
  • Ferritin & TSAT every 1-3 months
  • BP – HTN most common AE reported; caution if BP uncontrolled

Year 3 - Clinical (30 decks)

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