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clinical pathology > Anemia intro, blood loss, hypo/micro > Flashcards

Anemia intro, blood loss, hypo/micro Flashcards

1
Q

anemia (general)

A

decreased oxygen-carrying capacity of the blood leading to tissue hypoxia
-decreased RBC count
-decreased Hb (best value)

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2
Q

general anemia s/s

A

fatigue, pallor, dizziness, headache, weakness, dyspnea

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3
Q

anemia CBC findings

A

low RBC count, low Hb, low Hct

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4
Q

peripheral blood smear

A

most important single test in diagnosis of anemia–color, shape, size

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5
Q

RBC indices

A

MCV: size, 80-100, low=microcytic, high=macrocytic
MCH
MCHC: low=hypochromic, high=hyperchromic

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6
Q

RDW

A

earliest indicator of anemia, NL 11-15%, only increases

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7
Q

etiologic classifications of anemia

A

blood loss, deficient erythropoiesis, excessive RBC destruction

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8
Q

what are the two types of anemia due to blood loss?

A

acute post-hemorrhagic anemia
chronic post-hemorrhagic anemia

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9
Q

acute post-hemorrhagic anemia etiology

A

traumatic/spontaneous rupture of major blood vessel, erosion of artery by lesion, failure of hemostasis

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10
Q

acute post-hemorrhagic anemia lab findings

A

during or immediately following hemorrhage: RBC, Hb, Hct are normal
tissue fluid will enter circulation: drop in RBC count, Hb, and Hct
neutrophilic leukocytosis & thrombocytosis within hours
after several days: polychromatophilia, slight macrocytosis, occasional normoblasts, immature WBCs

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11
Q

treatment of acute post-hemorrhagic anemia

A

restoring iron stores (same as iron deficiency anemia)

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12
Q

etiology of chronic post-hemorrhagic anemia

A

prolonged moderate blood loss, GI tract lesion, urologic, gynecologic site

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13
Q

clinical findings for chronic post-hemorrhagic anemia

A

same as IDA

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14
Q

GI tract causes of chronic blood loss anemia

A

peptic ulcers, GERD, gastritis, colorectal cancer, polyps, hemorrhoids, crohn’s

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15
Q

GU reasons for chronic blood loss anemia

A

cancer along urinary tract (bladder cancer)

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16
Q

reproductive system causes of chronic blood loss anemia

A

heavy menses, hormonal imbalances, PCOS, endometriosis, PID, fibroids, endometrial cancers, hypothyroidism

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17
Q

hypochromic microcytic anemia DDx

A

iron deficiency anemia, sideroblastic anemia (iron utilization), anemia of chronic disease (iron re-utilization), thalassemia

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18
Q

normocytic normochromic anemia DDx

A

renal disease, endocrine failure, aplastic anemia, myelophthisic anemia

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19
Q

megaloblastic/macrocytic anemia DDx

A

B12/folate deficiency

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20
Q

types of anemia due to deficient erythropoiesis

A

hypo/micro, normo/normo, macro

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21
Q

anemia due to excessive RBC destruction

A

anemia due to intrinsic RBC defects
anemia due to extrinsic RBC defects

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22
Q

anemia due to intrinsic RBC defects

A

anemia due to red cell membrane alterations (hereditary spherocytosis)
anemia due to disorders of red cell metabolism (G6PD)
anemia due to defective hemoglobin synthesis (sickle cell, thalassemia)

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23
Q

anemia due to extrinsic RBC defects

A

traumatic hemolytic anemia, hemolysis due to infectious agent (malaria), anemia due to immunologic abnormalities (autoimmune attack)

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24
Q

CBC and RBC indices findings for hypochromic/microcytic anemia

A

Decreased Hb, Hct, RBC count
Decreased MCV, MCH, MCHC

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25
Q

Components of an iron panel

A

Serum ferritin: storage form of iron
Serum Iron: total iron in blood, bound to transferrin
Transferrin/total iron binding capacity (TIBC)
Iron saturation %: how much iron occupies transferrin

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26
Q

Iron metabolism

A

-Absorption of iron occurs in duodenum and proximal jejunum
-To be reabsorbed iron must be in ferrous state or bound to heme
-Iron from plants is in ferric state and must be converted to ferrous iron
-Bone marrow RBC precursors utilize portion of available iron
-The remainder is stored as ferritin or hemosiderin

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27
Q

What is hemosiderin?

A

Coagulation of ferritin

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28
Q

What is the most common type of anemia?

A

Iron deficiency anemia

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29
Q

General info about IDA

A

60% of anemias in people >65
Populations to watch: infants whose major source of nutrition is cow’s milk and juices, adolescent females, pregnancy, elderly

30
Q

Etiology of IDA

A

Iron intake not sufficient to replace normal losses
Iron not available for erythropoiesis adequate intake
Increased loss of body iron not adequately replaced by normal intake

31
Q

Risk factors for iron intake not sufficient to replace normal iron losses (either decrease in intake or increase in demand)

A

6mo-1yr: growth
Adolescent females: 1st period, growth, diet
Pregnancy: growth, peak in 3rd trimester
Elderly: insufficient dietary intake, dental issues, decreased stomach acid
Pica: cause & symptom; weird cravings (clay, dirt), vegetarians

32
Q

Risk factors for iron not available for erythropoiesis despite adequate intake (decrease absorption)

A

Malabsorption diseases: celiac, gastroectomy, chronic diarrhea
Achlorhydria: gastric bypass, antacids

33
Q

Risk factors for increased loss of body iron not adequately replaced by normal intake (blood loss)

A

Excessive blood loss: GI, carcinoma, hemorrhoids, vaginal
Excessive blood donation

34
Q

Step 1 in pathophysiology of IDA

A

Iron depletion; iron deficient, not anemic
Decrease in ferritin, NL Hb, NL RBC indices

35
Q

Step 2 in pathophysiology of IDA

A

Iron deficient erythropoiesis
Iron panel abnormalities present, changes in RBC indices—1st increase in RDW, decrease in MCV

36
Q

3rd step in pathophysiology of IDA

A

Iron deficiency anemia
Decrease in Hb, Hct, RBC count
S/s of anemia present

37
Q

What is pagophagia?

A

Craving for ice

38
Q

Clinical findings in IDA

A

Pallor, koilonychia, cheilosis
Neurological, restless leg syndrome, s/s of underlying condition

39
Q

What labs to order when suspecting hypo/micro anemia

A

CBC with differential blood smear, iron panel
Possibly: colonoscopy, endoscopy, fecal blood occult

40
Q

CBC findings in IDA

A

Decreased RBC count/Hb/Hct
Decreased MCV/MCH/MCHC
Increased RDW

41
Q

Iron panel findings in IDA

A

Decreased ferritin
Decreased serum iron
Increased transferrin/TIBC
Decreased iron saturation

42
Q

Special tests for IDA

A

Stainable iron in bone marrow aspiration, occult blood in stool, UA

43
Q

Management for IDA

A

Search for the cause and correct it
Heme vs non-heme iron

44
Q

Heme iron

A

Bound to myoglobin/hemoglobin from animal sources

45
Q

Non-heme iron

A

Less effective, most common supplement, plants

46
Q

Typical approach to management with non-heme iron salts

A

150-200 mg of elemental iron/day, doses split throughout the day
Ferrous sulphate: 325 mg 3x/day
Ferrous fumerate, ferrous gluconate, ferrous biscuit-glycinate all have differential elemental iron content, so dosage will vary

47
Q

Alternative approach to management with non-heme iron salts

A

Double dose, every other day
Can decrease side effects, but slow hemoglobin response

48
Q

Side effects of non-heme iron salts

A

Epigastric pain, nausea, darkened stool, diarrhea or constipation
Lead to non-compliance

49
Q

Risks/benefits of heme iron

A

More expensive, easier to absorb, not for vegetarians or vegans, complications with long term use that may lead to stroke or heart attack, not common
30/40 mg/day

50
Q

Other factors impacting iron treatment

A

Empty stomach: take 30 min before or 2 hrs after meal
Vitamin C enhances absorption
Calcium, manganese, copper, zinc, coffee, tea, antacids, PPIs, H2 blockers all interfere with iron absorption

51
Q

Food sources for iron

A

Red meat, liver, fish (heme)
Beans, green leafy vegetables, dried fruits, whole-grain and enriched breads (non-heme form that needs to be converted)

52
Q

Response to care for IDA

A

Reticulocyte count: 7-10 days after treatment
Hemoglobin should rise: 2 weeks
Continue treatment for 3-6 months to replenish iron stores

53
Q

General info on sideroblastic (iron utilization) anemia

A

Due to inadequate or abnormal utilization of Intracellular iron for hemoglobin synthesis, iron levels within mitochondria of RBC precursors are adequate or elevated
Rare

54
Q

Etiology of sideroblastic anemia

A

Hereditary
Acquired: primary—idiopathic, secondary—alcoholism, toxin induced (lead poisoning), nutritional deficiency (B6)

55
Q

Clinical findings for iron utilization anemia

A

Moderate to severe anemia, hepatosplenomegaly

56
Q

CBC findings for iron utilization anemia

A

Hypochromic, microcytic anemia, high RDW

57
Q

Iron panel findings for iron utilization anemia

A

Increase ferritin
Increase serum iron
NL/decrease TIBC
Increase iron saturation

58
Q

Peripheral blood smear findings of sideroblastic anemia

A

Ringed sideroblasts

59
Q

Chem panel findings for sideroblastic anemia

A

Liver enzymes elevated

60
Q

Special tests for sideroblastic anemia

A

Low reticulocyte count, bone marrow examination to confirm diagnosis (sideroblasts)

61
Q

Treatment of iron utilization anemia

A

Specific to cause, alcohol use
Supplementation of B6 in addition to treating the cause

62
Q

General info on iron re-utilization anemia (anemia of chronic disease)

A

Second most common anemia in the world
Can also be normocytic normochromic

63
Q

Etiology of ACD

A

Chronic infections, inflammatory diseases (RA, lupus), certain malignancies (liver, lung, breast cancer, lymphoma, multiple myeloma)

64
Q

Clinical findings for ACD

A

Anemia symptoms
Underlying disease symptoms

65
Q

CBC findings for ACD

A

Anemia, NL or slight elevation in RDW

66
Q

Iron panel findings for ACD (hypo/micro)

A

Increase ferritin
Decrease serum iron
Decrease transferrin
Decrease iron saturation

67
Q

Iron panel findings for ACD (normo/normo)

A

Increase ferritin
NL serum iron, transferrin, iron saturation

68
Q

Additional tests for ACD

A

CRP, ESR, other tests associated with primary condition

69
Q

Management of ACD

A

Treat underlying disease, decrease inflammation (longer process)

70
Q

Combined IDA and ACD

A

Difficult to identify due to acute phase reactants, serum transferrin receptor (elevated in IDA, NL in ACD), ferritin
After treatment of underlying inflammatory condition, if s/s and iron panel still indicate IDA, then go through treatment of IDA and follow-up accordingly

clinical pathology (6 decks)

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