Anemia intro, blood loss, hypo/micro Flashcards
anemia (general)
decreased oxygen-carrying capacity of the blood leading to tissue hypoxia
-decreased RBC count
-decreased Hb (best value)
general anemia s/s
fatigue, pallor, dizziness, headache, weakness, dyspnea
anemia CBC findings
low RBC count, low Hb, low Hct
peripheral blood smear
most important single test in diagnosis of anemia–color, shape, size
RBC indices
MCV: size, 80-100, low=microcytic, high=macrocytic
MCH
MCHC: low=hypochromic, high=hyperchromic
RDW
earliest indicator of anemia, NL 11-15%, only increases
etiologic classifications of anemia
blood loss, deficient erythropoiesis, excessive RBC destruction
what are the two types of anemia due to blood loss?
acute post-hemorrhagic anemia
chronic post-hemorrhagic anemia
acute post-hemorrhagic anemia etiology
traumatic/spontaneous rupture of major blood vessel, erosion of artery by lesion, failure of hemostasis
acute post-hemorrhagic anemia lab findings
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
treatment of acute post-hemorrhagic anemia
restoring iron stores (same as iron deficiency anemia)
etiology of chronic post-hemorrhagic anemia
prolonged moderate blood loss, GI tract lesion, urologic, gynecologic site
clinical findings for chronic post-hemorrhagic anemia
same as IDA
GI tract causes of chronic blood loss anemia
peptic ulcers, GERD, gastritis, colorectal cancer, polyps, hemorrhoids, crohn’s
GU reasons for chronic blood loss anemia
cancer along urinary tract (bladder cancer)
reproductive system causes of chronic blood loss anemia
heavy menses, hormonal imbalances, PCOS, endometriosis, PID, fibroids, endometrial cancers, hypothyroidism
hypochromic microcytic anemia DDx
iron deficiency anemia, sideroblastic anemia (iron utilization), anemia of chronic disease (iron re-utilization), thalassemia
normocytic normochromic anemia DDx
renal disease, endocrine failure, aplastic anemia, myelophthisic anemia
megaloblastic/macrocytic anemia DDx
B12/folate deficiency
types of anemia due to deficient erythropoiesis
hypo/micro, normo/normo, macro
anemia due to excessive RBC destruction
anemia due to intrinsic RBC defects
anemia due to extrinsic RBC defects
anemia due to intrinsic RBC defects
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)
anemia due to extrinsic RBC defects
traumatic hemolytic anemia, hemolysis due to infectious agent (malaria), anemia due to immunologic abnormalities (autoimmune attack)
CBC and RBC indices findings for hypochromic/microcytic anemia
Decreased Hb, Hct, RBC count
Decreased MCV, MCH, MCHC
Components of an iron panel
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
Iron metabolism
-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
What is hemosiderin?
Coagulation of ferritin
What is the most common type of anemia?
Iron deficiency anemia
General info about IDA
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
Etiology of IDA
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
Risk factors for iron intake not sufficient to replace normal iron losses (either decrease in intake or increase in demand)
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
Risk factors for iron not available for erythropoiesis despite adequate intake (decrease absorption)
Malabsorption diseases: celiac, gastroectomy, chronic diarrhea
Achlorhydria: gastric bypass, antacids
Risk factors for increased loss of body iron not adequately replaced by normal intake (blood loss)
Excessive blood loss: GI, carcinoma, hemorrhoids, vaginal
Excessive blood donation
Step 1 in pathophysiology of IDA
Iron depletion; iron deficient, not anemic
Decrease in ferritin, NL Hb, NL RBC indices
Step 2 in pathophysiology of IDA
Iron deficient erythropoiesis
Iron panel abnormalities present, changes in RBC indices—1st increase in RDW, decrease in MCV
3rd step in pathophysiology of IDA
Iron deficiency anemia
Decrease in Hb, Hct, RBC count
S/s of anemia present
What is pagophagia?
Craving for ice
Clinical findings in IDA
Pallor, koilonychia, cheilosis
Neurological, restless leg syndrome, s/s of underlying condition
What labs to order when suspecting hypo/micro anemia
CBC with differential blood smear, iron panel
Possibly: colonoscopy, endoscopy, fecal blood occult
CBC findings in IDA
Decreased RBC count/Hb/Hct
Decreased MCV/MCH/MCHC
Increased RDW
Iron panel findings in IDA
Decreased ferritin
Decreased serum iron
Increased transferrin/TIBC
Decreased iron saturation
Special tests for IDA
Stainable iron in bone marrow aspiration, occult blood in stool, UA
Management for IDA
Search for the cause and correct it
Heme vs non-heme iron
Heme iron
Bound to myoglobin/hemoglobin from animal sources
Non-heme iron
Less effective, most common supplement, plants
Typical approach to management with non-heme iron salts
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
Alternative approach to management with non-heme iron salts
Double dose, every other day
Can decrease side effects, but slow hemoglobin response
Side effects of non-heme iron salts
Epigastric pain, nausea, darkened stool, diarrhea or constipation
Lead to non-compliance
Risks/benefits of heme iron
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
Other factors impacting iron treatment
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
Food sources for iron
Red meat, liver, fish (heme)
Beans, green leafy vegetables, dried fruits, whole-grain and enriched breads (non-heme form that needs to be converted)
Response to care for IDA
Reticulocyte count: 7-10 days after treatment
Hemoglobin should rise: 2 weeks
Continue treatment for 3-6 months to replenish iron stores
General info on sideroblastic (iron utilization) anemia
Due to inadequate or abnormal utilization of Intracellular iron for hemoglobin synthesis, iron levels within mitochondria of RBC precursors are adequate or elevated
Rare
Etiology of sideroblastic anemia
Hereditary
Acquired: primary—idiopathic, secondary—alcoholism, toxin induced (lead poisoning), nutritional deficiency (B6)
Clinical findings for iron utilization anemia
Moderate to severe anemia, hepatosplenomegaly
CBC findings for iron utilization anemia
Hypochromic, microcytic anemia, high RDW
Iron panel findings for iron utilization anemia
Increase ferritin
Increase serum iron
NL/decrease TIBC
Increase iron saturation
Peripheral blood smear findings of sideroblastic anemia
Ringed sideroblasts
Chem panel findings for sideroblastic anemia
Liver enzymes elevated
Special tests for sideroblastic anemia
Low reticulocyte count, bone marrow examination to confirm diagnosis (sideroblasts)
Treatment of iron utilization anemia
Specific to cause, alcohol use
Supplementation of B6 in addition to treating the cause
General info on iron re-utilization anemia (anemia of chronic disease)
Second most common anemia in the world
Can also be normocytic normochromic
Etiology of ACD
Chronic infections, inflammatory diseases (RA, lupus), certain malignancies (liver, lung, breast cancer, lymphoma, multiple myeloma)
Clinical findings for ACD
Anemia symptoms
Underlying disease symptoms
CBC findings for ACD
Anemia, NL or slight elevation in RDW
Iron panel findings for ACD (hypo/micro)
Increase ferritin
Decrease serum iron
Decrease transferrin
Decrease iron saturation
Iron panel findings for ACD (normo/normo)
Increase ferritin
NL serum iron, transferrin, iron saturation
Additional tests for ACD
CRP, ESR, other tests associated with primary condition
Management of ACD
Treat underlying disease, decrease inflammation (longer process)
Combined IDA and ACD
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
