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Anemia Flashcards

1
Q

Thrombophilia

A

hypercoagulopathy, Thrombophilia is a risk factor for pathologic formation of an intravascular blood clot (thrombosis)

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2
Q

risk factors for thrombosis

A

stasis and vascular wall abnormalities, Thrombosis is usually a multifactorial condition

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3
Q

virchows triad

A

endothelial damage, hypercoaguability, stasis

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4
Q

Reasons for endothelial damage

A

smoking, htn, surgery, PICC lines, trauma

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5
Q

Reasons for hypercoaguability

A

heredity: factor V, prothrombin, protein C deficiency. acquired: cancer, chemo, pregnancy, obesity

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6
Q

Reasons for stasis

A

immobility, polycythemia

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7
Q

Inherited (autosomal dominant) causes

A

Protein C, protein S deficiency (inhibits f. V, VIII)

Factor V Leiden* most common (mutation f. V > resistance to inactivation)

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8
Q

Acquired causes

A

Malignancy (20% of all VTE occur in patients with cancer)
Pregnancy up to 2 months postpartum
Oral contraceptives or estrogen replacement therapy

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9
Q

Clinical features of inherited thrombophilia

A

Thrombosis before age < 50 years
Recurrent venous thrombosis DVT and PE
Family history of thrombosis before age 50
Thrombosis is more often when other factors are present (pregnancy, oral contraceptives, immobility)

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10
Q

Testing for inherited thrombophilia

A

ROUTINE thrombophilia testing is NOT recommended ( doesn’t affect management)
Available testing:
Protein C activity essay (abnormal in protein C deficiency)
Protein S activity essay (abnormal in protein S deficiency)
Protein C resistance essay (abnormal in factor V mutation)
PT/INR (normal)
Platelets (normal)

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11
Q

Thrombophilia therapy

A

Treat DVT/PE with anticoagulation therapy (Warfarin, direct oral anticoagulants ) for a minimum of 3 months (optimal length of the treatment is unknown)
IVC filter if there is a contraindication to anticoagulation

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12
Q

Anemia

A

Anemia is a deficits in the mass of circulating RBC ( the capacity to deliver oxygen is compromised) Measured as RBC count, concentration of Hgb (g/dl), % of Hct

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13
Q

What is hemoglobin

A

is a protein contained in RBC that is responsible for delivery of oxygen to the tissues Hct is a % of the volume of RBC in the total volume of a blood sample

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14
Q

Hgb: Hct

A

1:3

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15
Q

Normal Hgb

A

13.5-17.5 g/dl (male), 12-16 g/dl (female)

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16
Q

Hgb suggestive of anemia

A

Hgb concentration <14 g/dl in men and <12 g/dl in women suggests anemia

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17
Q

Symptoms of anemia

A

oxygen-caring capacity: tiredness, exercise intolerance, poor concentration, pallor, angina

cardiac compensation ( stroke volume, HR): palpitations, dyspnea on exertion, systolic murmur (hemic murmur)

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18
Q

Sx are minimal when

A

it is gradual and mild

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19
Q

MCV range

A

80-100

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20
Q

Microcytic

A

< 80

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21
Q

Macrocytic

A

> 100

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22
Q

Normocytic

A

80-100

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23
Q

Microcytic anemias (low MCV)

A

Small RBC (microcytosis) 90% of RBC volume composed of hgb. Hgb is a major contributor to the cell size Due to decreased production of Hgb

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24
Q

Hemoglobin made of

A

Made of Heme and Globin
Heme is mainly composed of iron ( that binds O2)
Reduction in any of these components will result in microcytic anemia

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25
Microcytic anemia etiology
Iron deficiency anemia (IDA) Anemia of chronic disease (ACD) Thalassemia
26
IDA
Most common reason for anemia worldwide Deficiency is due to dietary lack : meat (better absorption), sunflower seeds, nuts, whole grains, dark leafy greens poor iron absorption in duodenum (rare, Celiac disease) increased iron demands (pregnancy) blood loss (most common cause in adults, GI)
27
Manifestation of IDA -- iron deficiency
Pica (ice, clay) | Restless leg syndrome
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Manifestation of IDA -- Low hemoglobin
``` Tiredness Generalized weakness Shortness of breath Pallor Hemic murmur ```
29
Diagnosis of IDA: CBC is an initial test -- results on the CBC:
Low Hgb/Hct Low MCV < 80 fL Low MCHC (mean corpuscular hemoglobin concentration= the amount of Hgb per unit volume) < 33 g/dl Increased RDW (red cells distribution width) > 15% Low reticulocyte count
30
IDA blood smear
Low MCV on CBC MICROCYTOSIS on the blood smear | Low MCHC on CBC HYPOCHROMIA on blood smear
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IDA blood smear red blood cells
Increased RDW on CBC ANYSOCYTOSIS on blood smear
32
Diagnosis of IDA : iron study (diagnostic)
Low serum iron (N 50-150 ng/dl) Low ferritin (N 20-300 ng/dl) Low % transferrin saturation (N 20-50%) High TIBC (Total Iron Binding Capacity) (N 25-450 ng/dl) Low reticulocyte (“young cells” just released from bone marrow) count
33
Stages of IDA -- stage 1
(1) : Iron storage is depleted without causing anemia (ferritin) – asymptomatic
34
stage 2
(2) : Normocytic anemia (Hgb, normal MCV and normal reticulocyte count) – asymptomatic or mild symptoms of anemia
35
stage 3
(3) : Microcytic hypochromic anemia (low MCV, low MCHC, low reticulocyte count)- symptomatic
36
Management of IDA
Determine ETIOLOGY of iron deficiency and bleeding: History of menorrhagia/ abnormal uterine bleeding, melena, hematochezia, hematuria No obvious source of bleeding, consider occult GI bleeding (fecal occults blood, upper endoscopy, colonoscopy)
37
Severely symptomatic patients (myocardial ischemia)
RBC transfusion
38
Stable patients can get this
Oral iron supplementation (IV iron if absorption problems, intolerable GI effects of oral iron)
39
Oral iron supplementation side effects
``` nausea, constipation, heartburn, black stool Safe handling ( in a locked cabinet) : iron supplements account for 30% of fatal medication overdoses in children ```
40
Absorption is optimal if taken
30 min before meals with ascorbic acid (absorption can be reduced by 40-50% if taken with food)
41
How long is iron treatment for
Treat for 4-6 months or until ferritin level is normalized
42
Oral iron supplementation -- what increases absorption?
Vitamin C (orange juice)
43
Oral iron supplementation -- what decreases absorption?
``` Antacids Caffeine Calcium and calcium-containing foods (milk) H2 blockers PPIs ```
44
Response to iron supplementation, an increase in reticulocyte count (7-10 days) Is a response by the
marrow
45
increased Hgb (1-2 months into treatment ) indicates what
resolution of anemia
46
increased ferritin (4 months into treatment) indicates what
restoration of iron stores
47
Screening for IDA
Asymptomatic pregnant women should be screened for IDA at the first prenatal visit : Anemia on screening 60 to 120 mg of oral iron per day No anemia 30 mg/day of oral iron as primary prevention
48
Anemia of chronic disease (ACD)
Inflammatory mediators keep iron is storage sites (liver) Low available iron> low Heme > low Hgb> microcytic anemia Functional iron deficiency ( iron unavailable for erythropoiesis)
49
Anemia of chronic disease (ACD) causes
``` chronic infection (TB, HIV, osteomyelitis) cancer chronic inflammation ( RA, SLE) chronic kidney disease (+ erythropoietin deficiency) ```
50
Diagnosis of ACD : CBC (initial test)
Normal MCV ( initially) >> low MCV Low Hgb/ Hct Normal MCHC (initially) >> low MCHC Normal RDW
51
Diagnosis of ACD: iron studies (diagnostic test)
Elevated ferritin Low TIBC Elevated transferrin saturation Low serum iron
52
Management of ACD
Treat underlying disease
53
Thalassemia
Inherited genetic disorder Inadequate PRODUCTION of globin> low Hgb> microcytic anemia
54
Thalassemia subtypes
Alfa and Beta
55
Alpha thalassemia
Genes that code for alpha globin are affected (inadequate production of alpha chains)
56
Beta thalassemia
Genes that code for beta globin are affected (inadequate production of beta chains)
57
Alpha chains are encoded by
4 genes (2 genes from mother, 2 from father) Severity of anemia depends of number of deleted genes (1 gene deleted – asymptomatic, 4 genes absent --incompatible with life)
58
Beta chains are encoded by
2 genes (1 from mother, 1 from father) Autosomal recessive inheritance. Severity of anemia variable: one abnormal gene – mild disease, two abnormal genes—moderate to severe
59
Thalassemia minor s/s
Asymptomatic | Signs of anemia
60
Thalassemia major s/s
Transfusion-depended anemia Symptoms appear within first year of life: severe anemia , failure to thrive, irritability, pallor, bones hyperplasia and deformities. Average life expectancy is 17 years
61
Beta thallasemia bone changes
Bone medullar expansion>> deformities (“chipmunk face”)
62
Diagnosis of thalassemia initial diagnostic testing
``` CBC: VERY Low MCV Low Hgb normal RDW (all produced cells are small) Iron studies: NORMAL ```
63
Most accurate thalassemia testing to diagnose
Hgb electrophoresis (separate chains) to confirm the diagnosis
64
Mgmt thal. minor
Usually no treatment necessary, genetic counseling
65
Mgmt thal. major
transfusion-dependent (+ chelation therapy to prevent iron overload)
66
Macrocytic anemias
MCV > 100 fL “Bad DNA“ Not enough material for DNA synthesis and replication > arrest of cellular division> macrocytic anemia (immature cells are larger) Normal iron, Hgb synthesis is not affected > normochromic (normal MCHC) RDW increased
67
Major causes of macrocytic anemia
Folate deficiency Vitamin B12 (cobalamin) deficiency Alcoholism Hypothyroidism
68
Dietary sources of b12
Meat, fish and milk (Only animal products ! ) Dietary deficiency in strict vegans Stores are large (3 years)
69
Folate sources
Animal and non-animal products including green leafy vegetables, beans, fruits (bananas), mushrooms, yeast Stores are limited (3 months)
70
causes of b12 deficiency
Malabsorption due to deficiency of intrinsic factor (pernicious anemia) –most common cause, Malabsorption due to gastric, bariatric, ileac surgery or Crohn’s disease
71
Causes of folate deficiency
Dietary lack (elderly and alcoholics, “ tea and toast” diet) - most common cause Malabsorption (absorbed in jejunum) Increased demand (pregnancy, cancer ) Drugs (methotrexate, antiepileptic drugs, Bactrim)
72
Pernicious anemia
Autoimmune disease Autoimmune destruction of parietal cells > IF deficiency > Vit B12 deficiency Because B12 is efficiently stored, it takes 2-3 years to develop anemia
73
Folate deficiency and pregnancy
Folate deficiency is teratogenic Associated w/ neural tube defect ( spina bifida) Recommendation: women planning pregnancy ( capable of conception) 0.4-0.8 mg/d for 3 month prior to conception
74
Women who has hx of giving birth to a child w. neural tube defect
4 mg/d 3 month before conception through 3 months of pregnancy
75
b12 deficiency manifestations
weakness, fatigue, atrophic glossitis, stomatitis Neurological (parasthesia first , ataxia, loss of vibratory sense, + Romberg sign, dementia )
76
Folate deficiency manifestations
weakness, fatigue, atrophic glossitis, stomatitis
77
dx b12 deficiency
MCV > 100 fL, low RBC Low reticulocyte count Low serum B12 Elevated serum methylmalonic acid (B12 breaks out methylmalonic acid)
78
dx Folate deficiency
MCV > 100 fL, low RBC Low reticulocyte count Low serum folate Normal level of methylmalonic acid
79
tx b12 deficiency
Parenteral (IM) therapy weekly > monthly (malabsorption) for the rest of life Watch for hypokalemia Hematological response is rapid ( retic.count 7 days). Full hematologic recovery takes 2 months Neurological changes are irreversible if prolonged
80
tx folate deficiency
Oral folate replacement daily (1 mg po daily) | Hematologic response is rapid
81
Normocytic anemias
Normal MCV Normal iron studies Low RBC, low Hgb
82
Normocytic anemias definition
Destruction of RBCs or loss of RBCs due to: Hemolysis (sickle cell anemia, autoimmune hemolytic anemia) Acute blood loss
83
Hemolytic anemias symptoms
Weakness, tiredness, pallor | Jaundice
84
Lab values hemolytic anemia
``` Normal MCV Low hemoglobin Elevated reticulocyte count Elevated indirect bilirubin Elevated LDH ```
85
Sickle cell disease (SCD)
Inheritance of abnormal (mutated) gene of beta chain of Hgb >> abnormal beta chain structure not quantity. Autosomal recessive: two beta chains are abnormal disease, one beta chain is abnormal  trait
86
SC trait manifestations
SC trait individuals carriers only one abnormal gene | Clinically asymptomatic
87
SCD diagnosis
Blood smear to detect red blood sickle cell (initial) | Electrophoresis to detect HgS (most accurate)
88
SCD treatment
Exchange blood transfusions for serious complications (stroke, acute chest syndrome, priapism) Vaccinations (pneumococcal, meningococcal, Hemophylus influenza) Hydroxyurea (increases HgF level) – reduces sickling episodes. Painful crises- hydration, oxygenation, pain control. Genetic counseling for carriers (SCD trait)
89
Hydroxyurea increases
fetal hgb

AGPC 4!!!!!! (10 decks)

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