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AGPC 4!!!!!! > Anemia > Flashcards

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
Q

Microcytic anemia etiology

A

Iron deficiency anemia (IDA)
Anemia of chronic disease (ACD)
Thalassemia

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26
Q

IDA

A

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)

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27
Q

Manifestation of IDA – iron deficiency

A

Pica (ice, clay)

Restless leg syndrome

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28
Q

Manifestation of IDA – Low hemoglobin

A 
Tiredness 
Generalized weakness 
Shortness of breath 
Pallor
Hemic murmur
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29
Q

Diagnosis of IDA: CBC is an initial test – results on the CBC:

A

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

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30
Q

IDA blood smear

A

Low MCV on CBC MICROCYTOSIS on the blood smear

Low MCHC on CBC HYPOCHROMIA on blood smear

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31
Q

IDA blood smear red blood cells

A

Increased RDW on CBC ANYSOCYTOSIS on blood smear

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32
Q

Diagnosis of IDA : iron study (diagnostic)

A

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

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33
Q

Stages of IDA – stage 1

A

(1) : Iron storage is depleted without causing anemia (ferritin) – asymptomatic

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34
Q

stage 2

A

(2) : Normocytic anemia (Hgb, normal MCV and normal reticulocyte count) – asymptomatic or mild symptoms of anemia

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35
Q

stage 3

A

(3) : Microcytic hypochromic anemia (low MCV, low MCHC, low reticulocyte count)- symptomatic

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36
Q

Management of IDA

A

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
Q

Severely symptomatic patients (myocardial ischemia)

A

RBC transfusion

38
Q

Stable patients can get this

A

Oral iron supplementation (IV iron if absorption problems, intolerable GI effects of oral iron)

39
Q

Oral iron supplementation side effects

A 
nausea, constipation, heartburn, black stool
Safe handling ( in a locked cabinet) : iron supplements account for 30% of fatal medication overdoses in children
40
Q

Absorption is optimal if taken

A

30 min before meals with ascorbic acid (absorption can be reduced by 40-50% if taken with food)

41
Q

How long is iron treatment for

A

Treat for 4-6 months or until ferritin level is normalized

42
Q

Oral iron supplementation – what increases absorption?

A

Vitamin C (orange juice)

43
Q

Oral iron supplementation – what decreases absorption?

A 
Antacids 
Caffeine
Calcium and calcium-containing foods (milk)  
H2 blockers 
PPIs
44
Q

Response to iron supplementation, an increase in reticulocyte count (7-10 days) Is a response by the

A

marrow

45
Q

increased Hgb (1-2 months into treatment ) indicates what

A

resolution of anemia

46
Q

increased ferritin (4 months into treatment) indicates what

A

restoration of iron stores

47
Q

Screening for IDA

A

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
Q

Anemia of chronic disease (ACD)

A

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
Q

Anemia of chronic disease (ACD) causes

A 
chronic infection (TB, HIV, osteomyelitis)
cancer 
chronic inflammation ( RA, SLE)
chronic kidney disease (+ erythropoietin deficiency)
50
Q

Diagnosis of ACD : CBC (initial test)

A

Normal MCV ( initially) &raquo_space; low MCV
Low Hgb/ Hct
Normal MCHC (initially)&raquo_space; low MCHC
Normal RDW

51
Q

Diagnosis of ACD: iron studies (diagnostic test)

A

Elevated ferritin
Low TIBC
Elevated transferrin saturation
Low serum iron

52
Q

Management of ACD

A

Treat underlying disease

53
Q

Thalassemia

A

Inherited genetic disorder

Inadequate PRODUCTION of globin> low Hgb> microcytic anemia

54
Q

Thalassemia subtypes

A

Alfa and Beta

55
Q

Alpha thalassemia

A

Genes that code for alpha globin are affected (inadequate production of alpha chains)

56
Q

Beta thalassemia

A

Genes that code for beta globin are affected (inadequate production of beta chains)

57
Q

Alpha chains are encoded by

A

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
Q

Beta chains are encoded by

A

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
Q

Thalassemia minor s/s

A

Asymptomatic

Signs of anemia

60
Q

Thalassemia major s/s

A

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
Q

Beta thallasemia bone changes

A

Bone medullar expansion» deformities (“chipmunk face”)

62
Q

Diagnosis of thalassemia initial diagnostic testing

A 
CBC: 
VERY Low MCV 
Low Hgb 
normal RDW (all produced cells are small)
Iron studies: NORMAL
63
Q

Most accurate thalassemia testing to diagnose

A

Hgb electrophoresis (separate chains) to confirm the diagnosis

64
Q

Mgmt thal. minor

A

Usually no treatment necessary, genetic counseling

65
Q

Mgmt thal. major

A

transfusion-dependent (+ chelation therapy to prevent iron overload)

66
Q

Macrocytic anemias

A

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
Q

Major causes of macrocytic anemia

A

Folate deficiency
Vitamin B12 (cobalamin) deficiency
Alcoholism
Hypothyroidism

68
Q

Dietary sources of b12

A

Meat, fish and milk (Only animal products ! )
Dietary deficiency in strict vegans
Stores are large (3 years)

69
Q

Folate sources

A

Animal and non-animal products including green leafy vegetables, beans, fruits (bananas), mushrooms, yeast
Stores are limited (3 months)

70
Q

causes of b12 deficiency

A

Malabsorption due to deficiency of intrinsic factor (pernicious anemia) –most common cause, Malabsorption due to gastric, bariatric, ileac surgery or Crohn’s disease

71
Q

Causes of folate deficiency

A

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
Q

Pernicious anemia

A

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
Q

Folate deficiency and pregnancy

A

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
Q

Women who has hx of giving birth to a child w. neural tube defect

A

4 mg/d 3 month before conception through 3 months of pregnancy

75
Q

b12 deficiency manifestations

A

weakness, fatigue, atrophic glossitis, stomatitis

Neurological (parasthesia first , ataxia, loss of vibratory sense, + Romberg sign, dementia )

76
Q

Folate deficiency manifestations

A

weakness, fatigue, atrophic glossitis, stomatitis

77
Q

dx b12 deficiency

A

MCV > 100 fL, low RBC
Low reticulocyte count
Low serum B12
Elevated serum methylmalonic acid (B12 breaks out methylmalonic acid)

78
Q

dx Folate deficiency

A

MCV > 100 fL, low RBC
Low reticulocyte count
Low serum folate
Normal level of methylmalonic acid

79
Q

tx b12 deficiency

A

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
Q

tx folate deficiency

A

Oral folate replacement daily (1 mg po daily)

Hematologic response is rapid

81
Q

Normocytic anemias

A

Normal MCV
Normal iron studies
Low RBC, low Hgb

82
Q

Normocytic anemias definition

A

Destruction of RBCs or loss of RBCs due to: Hemolysis (sickle cell anemia, autoimmune hemolytic anemia)
Acute blood loss

83
Q

Hemolytic anemias symptoms

A

Weakness, tiredness, pallor

Jaundice

84
Q

Lab values hemolytic anemia

A 
Normal MCV
Low hemoglobin 
Elevated reticulocyte count 
Elevated indirect bilirubin 
Elevated LDH
85
Q

Sickle cell disease (SCD)

A

Inheritance of abnormal (mutated) gene of beta chain of Hgb&raquo_space; abnormal beta chain structure not quantity. Autosomal recessive: two beta chains are abnormal disease, one beta chain is abnormal  trait

86
Q

SC trait manifestations

A

SC trait individuals carriers only one abnormal gene

Clinically asymptomatic

87
Q

SCD diagnosis

A

Blood smear to detect red blood sickle cell (initial)

Electrophoresis to detect HgS (most accurate)

88
Q

SCD treatment

A

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
Q

Hydroxyurea increases

A

fetal hgb

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

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