week 12-anemia Flashcards

1
Q

anemia definition

A

lower than normal level of healthy red blood cells or hemoglobin

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2
Q

anemia is characterized by (3)

A

ow hemoglobin, low hematocrit, low RBC count on the complete blood count (CBC)

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3
Q

anemia in adult males hemoglobin and hematocrit values

A

Anemia in adult males: hemoglobin <130 g/L (13 g/dL); hematocrit <41%

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4
Q

anemia in adult females hemoglobin and hematocrit values

A

Anemia in nonpregnant adult females: hemoglobin <120 g/L (12 g/dL); hematocrit <36%

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5
Q

RBC count

A

The number of RBCs per volume of blood

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6
Q

hemoglobin

A

Amount of oxygen-carrying protein in the blood

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7
Q

hematocrit

A

Percentage of a given volume of whole blood occupied by packed RBCs

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8
Q

mean corpuscular volume MCV

A

Measurement of average size of RBCs

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9
Q

what has a larger MCV than RBCs

A

the reticulocytes are larger than mature RBCs

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10
Q

mean corpuscular hemoglobin

A

Amount of oxygen-carrying Hb inside RBCs

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11
Q

mean corpuscular hemoglobin concentration (MCHC)

A

Average concentration of Hb inside RBCs (i.e., ratio of MCH to MCV)

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12
Q

red cell distribution width (RDW)

A

Measurement of variance in RBC size

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13
Q

WBC count

A

The number of WBCs per volume of blood

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14
Q

WBC differential

A

Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils

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15
Q

platelet count

A

Number of platelets per volume of blood

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16
Q

mean platelet volume MPV

A

Measurement of average platelet size

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17
Q

reticulocytes

A

Immature RBCs that contain no nucleus but have residual RNA

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18
Q

symptoms of anemia

A

Symptoms in chronic anemia are due to decreased oxygen delivery to the body’s tissues:
* Fatigue
* Tachycardia
* Palpitations
* Dyspnea on exertion

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19
Q

what pallor spots have the highest LR for anemia

A

conjunctival rim pallor (LR+ 16.7)

palmar crease pallor (LR+ 7.9)

palmar pallor (LR+ 5.6)

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20
Q

what is the most important clinical sign for anemia but is not always evident until the hemoglobin drops quite low

A

Pallor is the most important clinical sign, but it is not usually visible unless hemoglobin falls to 80 g/L (8 g/dL)

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21
Q

are physical exams good to rule out anemia?

A
  • No physical sign rules out anemia
  • What does this mean?
  • Even without physical exam signs, order a complete blood count if your patient has symptoms that suggest anemia
  • Order a complete blood count if you observe conjunctival rim or palmar crease pallor
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22
Q

2 causes of anemia

A

reticulocytopenia

OR

reticulocytosis

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23
Q

reticulocytopenia

A

decreased RBC production

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24
Q

reticulocytosis

A

increased RBC destruction (hemolysis) or accelerated RBC loss

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25
Q

things that cause decreased RBC production (reticulocytopenia)

A
  • Hemoglobin synthesis lesion: iron deficiency, thalassemia, anemia of chronic disease, hypoerythropoietinemia
  • DNA synthesis lesion: megaloblastic anemia, folic acid deficiency, DNA synthesis inhibitor medications
  • Hematopoietic stem cell lesion: aplastic anemia, leukemia
  • Bone marrow infiltration: carcinoma, lymphoma, fibrosis, sarcoidosis, Gaucher disease, others
  • Immune-mediated inhibition: aplastic anemia, pure RBC aplasia
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26
Q

things that cause increased RBC destruction or accelerated RBC loss (reticulocytoisis)

A

Acute blood loss
* Hemolysis (intrinsic)
* Membrane lesion: hereditary spherocytosis, elliptocytosis
* Hemoglobin lesion: sickle cell, unstable hemoglobin
* Glycolysis lesion: pyruvate kinase deficiency
* Oxidation lesion: glucose-6-phosphate
dehydrogenase deficiency
* Hemolysis (extrinsic)
* Immune: warm antibody, cold antibody
* Microangiopathic: disseminated intravascular
coagulation, thrombotic thrombocytopenic purpura, hemolytic-uremic syndrome, mechanical cardiac valve, paravalvular leak
* Infection: Clostridium perfringens, malaria
* Hypersplenism

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27
Q

3 steps to a general approach to anemia

A
  1. Exclude acute blood loss
  2. Determine the general mechanism for anemia
    * Distinguish RBC underproduction from hemolysis
  3. Determine the specific cause of RBC underproduction or hemolysis
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28
Q

symptoms of acute blood loss

A
  • Hematemesis (vomit blood)
  • Melena (dark tar stool)
  • Hematochezia or rectal
    bleeding
  • Hematuria (blood in urine)
  • Menorrhagia or vaginal
    bleeding
  • Hemoptysis (cough up blood)
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29
Q

signs of acute blood loss

A
  • Hypotension
  • Tachycardia
  • Large ecchymoses (bruises)
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30
Q

what is a normal reticulocyte count

A

0.5-1.5%

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31
Q

what causes a low reticulocyte count

A

in RBC underproduction anemia

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32
Q

what causes a high reticulocyte count

A

in hemolysis or when bone marrow responds normally to blood loss

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33
Q

reticulocyte production index

A

Corrects the reticulocyte count for the degree of anemia and for the
prolonged peripheral maturation of reticulocytes that occurs in anemia

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34
Q

reticulocyte production index calculation

A
  • RPI = reticulocyte count % x (Hct/45) / Maturation
  • Maturation represents the maturation time of RBCs in days at various levels of anemia
  • Maturation = 1.0 for Hct ≥40%; Maturation = 1.5 for Hct 30-39.9%; Maturation = 2.0 for Hct 20-29.9%; Maturation = 2.5 for Hct <20%
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35
Q

what is a normal reticulocyte production index

A

1

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36
Q

in patients with anemia an RPI <2 indicates

A

hypo proliferative anemia
(RBC underproduction anemia)

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37
Q

in patients with anemia an RPI >2 indicates

A

hyperproliferative anemia (hemolysis or when
bone marrow responds normally to blood loss)

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38
Q

RPI >2 or <2

A

<2 = hypo proliferative anemia

> 2= hyper proliferative anemia

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39
Q

what is the normal range of MCV

A

80-100 fL

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40
Q

macrocytic anemia vs microcytic anemia

A

macro= * Average RBC is larger than normal

micro= * Average RBC is smaller than normal

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41
Q

2 subcategories of microcytic anemia

A
  • Subcategorized as megaloblastic (due to impaired DNA synthesis) or non-megaloblastic (normal DNA synthesis)
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42
Q

macrotyic anemia has an MCV of

A

> 100 fL

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43
Q

microcytic anemia has a MCV of

A

<80 fL

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44
Q

normocytic, microcytic, and microcytic anemia MCV values

A

normo= 80-100

macro= >100 fL

micro= <80 fL

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45
Q

types of normocytic anemia

A
  • Anemia of chronic disease/inflammation
  • Anemia of renal/kidney disease

and Mild form of most
acquired microcytic or macrocytic etiologies of anemia (i.e. early stages)

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46
Q

anemias of chronic disease/ inflammation can be 2 types of sizes

A

normocytic or microcytic

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47
Q

examples of microcytic anemia

A
  • Iron deficiency
  • Thalassemia
  • Anemia of chronic
    disease/inflammation
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48
Q

macrocytic (megaloblastic) and (non-megaloblastic anemias)

A

megaloblastic;
* Vitamin B12 deficiency
* Folate deficiency

non:
* Aplastic anemia
* Myelodysplastic
syndrome
* liver disease
* hypothyroidism

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49
Q

MCV and specificity?

A
  • MCV is not specific! Do not use RBC size alone to rule in/out a specific cause of anemia.
  • What about the rest of the red cell indices?
  • MCH and MCHC tend to trend with the MCV and are not particularly sensitive or specific
  • RDW is not sensitive or specific
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50
Q

what is the most common cause of anemia worldwide

A

iron defieincy anemia

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51
Q

what is the most common cause of microcytic anemia (low MCV)

A

iron deficiency anemia

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52
Q

80% of patients with microcytic anemia are from

A

chronic blood loss

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53
Q

prevalence in different groups for IDA

A
  • 1-2% in men <50 years of age
  • 10% in menstruating women
  • 3% in children aged 1-3
  • In United States: 7% in non-Hispanic White women; 20% in Mexican and Black women
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54
Q

2 most common causes of iron deficiency

A
  1. chronic blood loss
    a. GI bleeds
    b. heavy/frequent menses
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55
Q

causes of iron deficnicy anemia

A
  • Chronic blood loss
  • GI bleeds, heavy/frequent menses, blood donation, hemoglobinuria
  • Dietary deficiency (plant-based diets contain nonheme iron which has low bioavailability)
  • Decreased/impaired absorption
  • Autoimmune gastritis, celiac disease, Helicobacter pylori gastritis, inflammatory bowel disease, hereditary iron-refractory iron deficiency anemia, zinc deficiency
  • Increased requirements/demand * Children, pregnancy, lactation
  • Iron sequestration
  • Pulmonary hemosiderosis
  • Idiopathic
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56
Q

populations are risk of iron deficiency anemia

A
  • Premenopausal, menstruating women due to menorrhagia and chronic blood loss without proper iron supplementation
  • Men and postmenopausal women > age 50 due to colorectal cancer (occult blood loss from GI tract)
  • Non-breastfed preschool children on cow’s milk
  • Strict vegans/vegetarians
  • Low-income families; developing countries
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57
Q

signs and symptoms of iron deficiency anemia

A
  • Restless legs
  • Pica/pagophagia – craving for specific foods e.g., ice chips
  • Glossitis (inflamed tongue) (tender, smooth, red tongue)
  • Cheilitis (inflamed lips)
  • Brittle nails, koilonychia (spooning of nails)
  • Severe iron deficiency: dysphagia due to formation of esophageal webs (Plummer-Vinson syndrome)
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58
Q

size and colour in iron deficiency anemia

A

Typically presents as microcytic, hypochromic anemia on peripheral blood smear

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59
Q

what is the best biomarker for iron deficiency anemia

A

decreased serum ferritin

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60
Q

in iron deficiency anemia what happens to

-serum ferritin

-transferrin saturation

-serum iron

-total iron binding capacity

A
  • Decreased serum ferritin
  • Ferritin <15 ug/L (LR+ 51)
  • Ferritin <30 ug/L (LR+ 46)
  • Decreased transferrin saturation
  • Transferrin saturation ≤5% (LR+ 10.46)
  • Decreased serum iron
  • Increased total iron-binding capacity
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61
Q

what to do if this GI source of bleeding

A

fecal occult blood test

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62
Q

Serum transferrin receptor-ferritin index

A

Helps distinguish iron deficiency anemia from other causes when ferritin is midrange

i.e. serum ferritin is usually low in IDA but if there’s inflammation it can increase it

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63
Q

Serum transferrin receptor-ferritin index of < 1.5 and > 1.5 suggests what

A

> 1.5 = IDA
< 1.5 = other cause of anemia (i.e. chronic disease, like chronic kidney disease in elders)

64
Q

IDA treatment

A

-treat underlying cause
- oral iron or IV iron

65
Q

how long to replete iron stores and hemoglobin

A

6 months of iron therapy to replete iron stores; hemoglobin levels may return to normal by 6-8 weeks

66
Q

when to consider blood transfusion in IDA

A
  • Is hypotensive and actively bleeding
  • Has angina, dizziness, syncope, severe dyspnea or severe fatigue * Has very low hemoglobin <70 g/L (7 g/dL)
67
Q

what does b12 deficiency anemia cause

A

Causes megaloblastic macrocytic anemia (high MCV)

68
Q

MCV in b12 deficiency anemia

A

high

69
Q

b12 defieicny anemia is characterized by

A

Characterized by hypersegmented neutrophils on peripheral blood smear

70
Q

pathophysiology in b12 deficiency anemia

A
  • Vitamin B12 deficiency → impaired DNA synthesis → decreased RBC production
71
Q

risk factors for b12 deficiency

A

vegan diet, autoimmune diseases, elderly

72
Q

symptoms in b12 deficiency anemia

A

Presents with neurologic symptoms (paresthesias, sensory loss – especially vibration and position sense, ataxia)

73
Q

most common causes of b12 deficiency anemia

A
  • Food-cobalamin malabsorption (B12 not released from food protein due to impaired peptic digestion)
  • Affects up to 20% of older adults
  • Caused by atrophic gastritis and achlorhydria – can be due to chronic H. pylori infection, gastric surgery, long-term used of acid- suppressing medications
  • Lack of intrinsic factor
  • Caused by gastrectomy or pernicious anemia
  • Dietary vitamin B12 deficiency: vegan diet
74
Q

less common causes of b12 deficiency anemia

A
  • Malabsorption in terminal ileum
  • Caused by surgical removal or bypass, Crohn disease, celiac disease, or bacterial overgrowth
  • Drugs interfering with B12 absorption
  • Metformin, proton pump inhibitors, colchicine, ethanol, neomycin
  • Congenital disorders (e.g., transcobalamin II deficiency)
75
Q

b12 deficiency anemia is what type of anemia

A

pernicious anemia

76
Q

what is the autoimmune cause of b12 defieicny anemia called

A

pernicious anemia

77
Q

what is pernicious anemia causing b12 deficiency anemia

A

autoimmune; loss of IF

Perniciousanemia–autoimmune-mediatedgastricatrophy→lossofparietal cells→decreased secretion of intrinsic factor→decreased dietary vitamin B12 absorption

78
Q

who is pernicious anemia most common in

A

old, comorbid autoimmune disease

  • Most common in patients > age 50 (median age at diagnosis: 70-80 years; prevalence ~2%); Uncommon before age 30
  • 25% have a family history of pernicious anemia
  • 10% have autoimmune thyroid disease; higher incidence of other autoimmune
    disorders including diabetes mellitus type 1 and vitiligo
79
Q

how to diagnose pernicious anemia

A

test for the presence of anti-intrinsic factor
antibodies

80
Q

what are the levels of b12, homocysteine and methylmalonic acid in b12 deificney anemia

A

b12 is low
homocysteine and MMA are high

81
Q

what can cause b12 to be falsely low

A

folate deficiency, pregnancy, oral contraceptive use

82
Q

what can cause b12 to be falsely normal

A

myeloproliferative disorders ,liver disease, bacterial overgrowth syndromes

83
Q

why is homocysteine and methylmalonic acid high in b12 deficiency anemia

A

because you need b12 to turn homocysteine in methionine and for MMA into succinyl coa

84
Q

reasons for homocysteine elevation (not just b12 deficiency)

A

folate deficiency, chronic kidney disease, hypovolemia, hypothyroidism

85
Q

reasons for methylmalonic acid elevation (not just b12 deficiency)

A

chronic kidney disease, hypovolemia

86
Q

what is more specific for b12 deificney: homocysteine or methylmalonic acid (MMA)

A

MMA

87
Q

when to check for b12 deficiency

A

in folate deficiency

88
Q

b12 supplement

A
  • Reversible by restoring vitamin B12 through dietary intake, oral supplementation, parenteral supplementation
  • Response to therapy is another way to establish the presence of B12 deficiency
89
Q

b12 deficiency and folate deficiency anemia both present as

A

megaloblastic macrocytic anemia (high MCV)

90
Q

folate deficnicney is caused by

A

megaloblastic macrocytic anemia

91
Q

what is the MCV in folate deificny anemia

A

high

92
Q

what is folate deificny anemia characterized by

A

Characterized by hypersegmented neutrophils on peripheral blood smear

93
Q

pathophysiology of folate defiicney anemia

A

Folate deficiency → impaired DNA synthesis → decreased RBC production

94
Q

common causes of folate deificny anemia

A

alcohol abuse, increased folate demand due to pregnancy, sickle cell anemia, starvation/malnutrition, drugs (methotrexate, phenytoin, sulfalazine)

95
Q

folate levels and homocysteine levels in folate deficiency anemia

A

low folate

high homocysteine

96
Q

what test to differentiate between folate and b12 deificney anemia

A

increased homocysteine but normal MMA in folate deficiency

97
Q

what non-nutritional anemias may mimic folate of b12 deificny anemia

A
  • Anemia of renal disease
  • Anemia of chronic disease
  • Thalassemia
  • Myelodysplastic syndrome
98
Q

SLIDE 51 for comparing iron stores in anemias

A

DO!

99
Q

anemia of renal disease (kidney disease) what does it decrease the production of

A

EPO

  • Kidney disease→decreased erythropoietin (EPO) production→ decreased production of RBCs
100
Q

what type of size and colour anemia in anemia of renal disease

A

Usually normocytic normochromic anemia
* Microcytosis can occur

101
Q

clinical findings in anemia of renal disease

A

low EPO, low Hb, low iron

  • Low EPO levels
  • Usually normocytic normochromic anemia
  • Microcytosis can occur
  • Low hemoglobin concentrations (ranging from mild to severe depending on level of renal failure)
  • Variety of morphologic abnormalities
  • Low serum iron levels and percentage of iron saturation
  • Serum transferrin receptor-ferritin index <1.5 with increased creatinine and decreased GFR suggests anemia due to chronic
    kidney disease
102
Q

what is the 2nd most prevalent cause of anemia after iron deficiency anemia

A

anemia of chronic disease

103
Q

what is anemia of chronic disease associated with

A

infection, inflammation, malignancy, trauma

104
Q

what is impaired in anemia of chronic disease

A

Impaired iron transport from iron storage sites (e.g., liver, spleen, bone
marrow) to developing RBCs→decreased production of RBCs

105
Q

size and colour of anemia in anemia of chronic disease

A
  • Usually mild normocytic normochromic anemia, with time can evolve to mild microcytic hypochromic anemia
106
Q

clinical findings in anemia of chronic disease

A
  • Usually mild normocytic normochromic anemia, with time can evolve to mild microcytic hypochromic anemia
  • Nearly normal peripheral blood smear
  • Low serum iron with normal to increased iron stores
107
Q

CHARTT ON SLIDE 54 to DDX IDA and anemia of chronic diseas

A

important go look!

108
Q

other tests to consider in anemia of chronic disease

A
  • Liver enzymes if there is history of liver disease * Creatinine if there is history of kidney disease
  • Elevated inflammatory markers: ESR and CRP
  • If possible, treat the underlying chronic disease
109
Q

steps if suspect microcytic or normocytic anemia

A
  1. serum ferritin level
    (if low = IDA)
    (high= consider congenital hemoglobiopathies)
  2. if midrange then serum transferrin receptor ferritin index
    (>1.5= iron deficient, <1.5= continue)
  3. obtain basic metabolic panel and look for GFR to see if kidney disease or other unexpalin anemia of chronic disease

(FLOW CHART ON SLIDE 58)

110
Q

if serum ferritin is low midrange and elevated what to do if suspect anemia

A

low= above treamtent threshold; treat IDA

midrange= do serum transferrin receptor ferritin index (keep testing bc between treatment and testing threshold for IDA)

elevated= consider congenital hemoglobiopathies (below testing threshold for IDA)

111
Q

GFR for chronic kidney disease

A

<60

112
Q

basic metabolic panel to get GFR for kidney disease

A

Basic Metabolic Panel
(aka electrolyte panel or chemical screen)
* Glucose
* Calcium
* Sodium
* Potassium
* Carbon dioxide
* Chloride
* Blood urea nitrogen (BUN)
* Creatinine

113
Q

what is the most common inherited disorders

A

thalassemias

114
Q

what does a thalassemias do

A
  • Congenital abnormality of hemoglobin synthesis → decreased production of RBCs
115
Q

alpha vs beta thalassemia

A
  • α- Thalassemia – due to unbalanced synthesis of alpha globin chains * Highest prevalence of alpha-thalassemia mutations in persons of
    African, Mediterranean and Southeast Asian descent
  • β- Thalassemia – due to unbalanced synthesis of beta globin chains
  • Highest prevalence of beta-thalassemia mutations in persons of Mediterranean, Middle Eastern, and Southeast Asian descent
116
Q

1 severity of alpha thalassemia

A

1 defective/missing alpha gene = α- thalassemia minima
* Asymptomatic

117
Q

2 severity of alpha thalassemia

A
  • 2 defective/missing alpha genes = α- thalassemia minor
  • Mild anemia symptoms
118
Q

3 severity of alpha thalassemia

A

3 defective/missing alpha genes = Hemoglobin H disease
* Moderate to severe anemia symptoms

119
Q

4 severity of alpha thalassemia

A
  • 4 defective/missing alpha genes = hydrops fetalis with
    Hemoglobin Barts
  • Usually fatal in utero
  • Rare newborn survival requires lifelong blood transfusions
120
Q

type 1 of beta thalasemia

A

1 defective/missing beta gene = β- thalassemia
minor
* Mild anemia symptoms

121
Q

type 2 of beta thalassemia

A
  • 2 defective/missing beta genes
  • Moderate anemia symptoms = β- thalassemia intermedia
  • Severe anemia symptoms = β- thalassemia major (Cooley’s anemia)
122
Q

if 2 missing beta genes in beta thalasemia could be

A

b-thalassmeia intermedia of b-thalassemia major (Cooley’s anemia)

123
Q

what are the moderate to severe forms of thlassemisas

A

Moderate to severe forms of thalassemia (includes β- thalassemia intermedia, β-thalassemia major, and Hemoglobin H disease) are usually diagnosed in childhood

124
Q

what are the moderate to severe forms of thalassemias symptoms?

A
  • Severe anemia
  • Growth disturbances and delayed puberty * Bone abnormalities (e.g., osteoporosis)
  • Splenomegaly
  • Pallor or jaundice
125
Q

what are the mild forms of thalassemias

A

(includes β- thalassemia minor and α-thalassemia minor) may be unrecognized into adulthood and appear like a mild iron deficiency anemia

126
Q

size and colour of cell and other symptoms in mild forms of thalassemias

A
  • Mild hypochromic, microcytic anemia
  • May have splenomegaly (15-20%)
127
Q

diagnosing thalassemia

A
  • Look for a family history of anemia
  • Blood tests: CBC, peripheral blood smear
  • Hemoglobin electrophoresis
  • Genetic testing
128
Q

myelodysplastic syndrome

A

aka hyperplastic bone marrow with bone marrow failure, refractory anemia, smoldering leukemia, preleukemia

129
Q

pathophysiology of myelodysplastic syndrome

A

Blood cell components fail to mature → deficient production of mature cells into peripheral blood (including RBCs)

130
Q

risks for development of myelodysplastic syndrome

A
  • Increased risk with advancing age
  • Can be associated with preceding disorders such as malignancy or bone marrow dysfunction
  • May follow radiotherapy or chemotherapy
131
Q

5 subtypes of myelodysplastic syndrome

A
  1. Refractory anemia
  2. Refractory anemia with excess blasts
  3. Refractory anemia with leukemia in transformation 4. Refractory anemia with sideroblasts
  4. Chronic myelomonocytic leukemia

can all transform into acute leukemia, #3 the quickest

132
Q

what is the worst myelodysplastic syndrome and why

A

Refractory anemia with leukemia in transformation

Can transform into acute leukemia within months.

133
Q

what size of anemia in myelodysplastic syndrome

A

megaloblastic or microcytic anemia

134
Q

when to suspect myelodysplastic syndrome

A
  • Pancytopenia: anemia combined with abnormalities in one or two of the other marrow cell lines (WBCs, platelets)
  • Peripheral blood smear findings: abnormalities of
    RBC shape and size, polymorphonuclear leukocytes
    with hypersegmentation or Pelger-Huët nuclear
    anomaly (a bilobular polymorphonuclear leukocyte)
135
Q

pancytopenia in which anemia type

A

myelodysplastic syndrome

136
Q

a high reticulocyte count is suggestive of

A

High reticulocyte count and/or RPI > 2.0 suggests
hemolysis. It can also suggest normal bone marrow response to acute blood loss (but we already excluded
acute blood loss in step 1).

137
Q

hemolytic anemia? what is the size and MCV?

A

Normocytic anemia (MCV 80-100 fL) caused by destruction of RBCs

138
Q

cause of hemolytic anemia

A

Several ways to classify: acute vs. chronic disease, immune vs. non-immune mediated, intravascular vs. extravascular, inherited vs. acquired, and intracorpuscular vs. extracorpuscular

139
Q

inherited vs acquired causes of hemolytic anemia

A

Inherited/Hereditary
* Enzymopathies, disorders of hemoglobin (sickle cell), defects in red blood cell metabolism (G6PD deficiency, pyruvate kinase deficiency), defects in red blood cell membrane production (hereditary spherocytosis and elliptocytosis)

  • Acquired
  • Immune-mediated, infection, microangiopathic, blood transfusion-related, and secondary to hypersplenism
140
Q

extravascular vs intravascular hemolysis causing hemolytic anemia

A

extravascular= RBCs are prematurely removed from the circulation by the liver and spleen. This accounts for majority of cases of hemolytic anemia.

Intravascular hemolysis: RBCs lyse within the circulation. Less common.

141
Q

what is more common; intravascular or extravascular hemolysis

A

extravascualr

142
Q

causes of extravascular hemolysis

A
  • Hemoglobinopathies (sickle cell, thalassemias)
  • Enzymopathies (G6PD deficiency, pyruvate kinase deficiency)
  • Membrane defects (hereditary spherocytosis, hereditary elliptocytosis)
  • Drug-induced
143
Q

causes of intravascular hemolysis

A
  • Paroxysmal nocturnal hemoglobinuria (PHH)
  • Autoimmune hemolytic anemia (AIHA)
  • Transfusion reactions
  • Microangiopathic hemolytic anemia (MAHA)
  • Disseminated intravascular coagulation (DIC)
  • Infections
  • Snake bites/venom
144
Q

signs and symptoms of hemolytic anemia

A
  • General signs and symptoms of anemia: shortness of breath, weakness, fatigue, arrhythmias, tachycardia
  • Hemolysis may also lead to jaundice
  • Lymphadenopathy, hepatosplenomegaly
145
Q

hemolytic anemia with diarrhea vs with hematuria

A
  • Hemolytic anemia with diarrhea → consider hemolytic uremic syndrome
  • Hemolytic anemia with hematuria → consider paroxysmal nocturnal hemoglobinuria
146
Q
  • Hemolytic anemia with hematuria → consider
A
  • Hemolytic anemia with hematuria → consider paroxysmal nocturnal hemoglobinuria
147
Q
  • Hemolytic anemia with diarrhea → consider
A
  • Hemolytic anemia with diarrhea → consider hemolytic uremic syndrome
148
Q

what happens to the following labs in hemolytic anemia

  • reticulocyte
    -lactate dehydorgenase
    -unconjugated bilirubin
    haptoglobin
A
  • Elevated reticulocyte count
  • Increased lactate dehydrogenase (LDH)
  • Elevated unconjugated bilirubin
  • Decreased Haptoglobin
149
Q

exam of peripheral blood smear shows what in hemolytic anemia

A

abnormal RBC shapes (e.g., schistocytes, spherocytes, bite cells)

150
Q

to figure out if hemolytic anemia is immune mediated what test?

A

Direct antiglobulin (Coombs) test: warm and cold agglutins can differentiate whether the cause is immune-mediated

151
Q

maangment of hemolytic anemia

A
  • Workup and treatment requires interprofessional approach including referral to a hematologist
  • Treatment and outcomes vary depending on the underlying cause of hemolysis
152
Q

untreated anemia in pregnancy

A

premature labour and increased blood loss during birth; low birth weight and risk of anemia in baby

153
Q

untreated anemia in elderly

A

cardiac complications such as myocardial infarction, angina, arrhythmias, heart failure

154
Q

untreated anemia in kids

A

impaired neurological development (cognitive, mental, and developmental delays)

155
Q

interprofessional managen of anemia

A
  • Gastroenterologist if a gastrointestinal bleed is suspected
  • Nephrologist if anemia of chronic disease in the setting of renal failure is suspected
  • Hematologist if a bone marrow disorder is suspected
  • Gynecologist if intractable menorrhagia is suspected
  • Cardiologist if severe anemia leads to angina, myocardial infarction, heart failure, or arrhythmias