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DMD 5243 > Anemia (complete) > Flashcards

Anemia (complete) Flashcards

1
Q

What is anemia

A

a reduction below normal in hemoglobin or red blood cell number

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2
Q

What are the two components of a complete blood count (CBC)

A

Mean corpuscular volume (MCV)

Mean corpuscular hemoglobin concentration (MCHC)

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3
Q

What does the Mean Corpuscular Volume (MCV) measure

A

the size of the Red blood cell

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4
Q

What are the terms for a low, normal, and high MCV

A

low MCV = microcytic
normal MCV = Normocytic
high MCV = macrocytic

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5
Q

what does it mean if a RBC is macrocytic

A

that the RBC is abnormally large

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6
Q

what does it mean if a RBC is normocytic

A

that the RBC is the normal size

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7
Q

what does it mean if a RBC is microcytic

A

that the RBC is abnormally small

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8
Q

What does the Mean Corpuscular hemoglobin concentration (MCHC) measure

A

it measures the amount of hemoglobin in the RBC

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9
Q

What are the terms for low, normal, and high MCHC

A

low MCHC = hypochromic
normal MCHC = normochromic
high MCHC = DOESN’T HAPPEN

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10
Q

What does it mean if a RBC is hypochromic

A

that the RBC has an abnormally low hemoglobin concentration

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11
Q

what does it mean if a RBC is normochromic

A

that the RBC has a normal hemoglobin concentration

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12
Q

What are the three different types of abnormalities that a RBC can have

A
  1. Size varation
  2. Hemoglobin concentration
  3. Shape variation
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13
Q

what is the term for variation in RBC shape

A

poikilocytosis

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14
Q

What are the symptoms of anemia

A
  1. pale skin/mucus membranes
  2. jaundice (if hemolytic)
  3. breathlessness
  4. tachycardia
  5. dizziness
  6. fatigue
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15
Q

What symptom of anemia is specific to hemolytic anemia

A

Jaundice

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16
Q

What are the three main causes of anemia

A
  1. Blood loss
  2. Excessive RBC destruction
  3. Insufficient RBC production
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17
Q

What are the two types of reasons for excessive RBC destruction

A
  1. extracorpuscular reasons

2. intracorpuscular reasons

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18
Q

What are the three reasons for insufficient RBC production

A
  1. too little material
  2. too few erythroblasts
  3. not enough room
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19
Q

What is the specific cause of anemia caused by blood loss

A

trauma resulting in acute blood loss

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20
Q

anemia caused by acute blood loss due to trauma will result in an increase of what

A

reticulocytes

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21
Q

what are reticulocytes

A

immature RBCs

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22
Q

how long does it take a reticulocyte to develop into a mature RBC after it has left the bone marrow and entered the blood

A

about one day

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23
Q

What is the normal percentage of RBCs in the blood that are reticulocytes

A

1%

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24
Q

What are the two types of signs that we will see when a patient is suffering from anemia due to excessive destruction of RBCs

A

signs of the excessive destruction

signs of an increase in production of RBCs (due to anemia)

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25
Q

What are the three signs of destruction of RBC

A
  1. increased bilirubin
  2. increased LDH
  3. reduced haptoglobin
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26
Q

What are the two signs of increased production of RBCs

A
  1. increased reticulocytes

2. nucleated red cells in blood

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27
Q

what is the life span of RBCs

A

120 days

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28
Q

Where are RBC destroyed

A

the liver and the spleen (NOT KIDNEYS)

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29
Q

What are RBCs broken down into in the spleen and liver

A
  1. Globin

2. Heme

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30
Q

after RBCs are broken down in the spleen and liver what is the globin used for

A

the globin is used in Amino Acid formation

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31
Q

after RBCs are broken down in the spleen and the liver what is the Heme turned into

A
  1. bilirubin

2. Iron

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32
Q

the Heme group of RBCs are broken down into bilirubin and iron. Where is the iron used

A

liver
spleen
bone marrow

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33
Q

the Heme group of RBCs are broken down into bilirubin and iron. What happens to the bilirubin

A

it is taken to the liver where it is conjugated, then secreted with the bile.

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34
Q

Why is bilirubin conjugated in the liver?

A

because unconjugated bilirubin is toxic

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35
Q

How does bilirubin travel in the blood

A

with albumin as the bilirubin-albumin complex

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36
Q

how is unconjugated bilirubin harmful

A

it damages cell membranes

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37
Q

what allows unconjugated bilirubin to be harmful to cell membranes

A

it is fat soluble

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38
Q

What is the enzyme that takes unconjugated bilirubin and conjugates it so that it is no longer toxic

A

glucoronyl transferase

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39
Q

What are the possible routes that bilirubin can take after it is excreted from the liver with bile

A
  1. it can be eliminated from the body with fecal matter
  2. it can be converted into urobilinogen and excreted in fecal matter
  3. it can be converted into urobilinogen and reabsorbed into the blood
  4. it can be converted into urobilinogen and excreted in the urine
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40
Q

What happens to the uronilinogen that is reabsorbed into the blood

A

it is taken back to the liver where it is further metabolized, and then will be secreted with bile again and eliminated in either the urine or feces

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41
Q

What happens if we have excess bilirubin in the body

A

a patient with too much bilirubin will get jaundice

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42
Q

what is jaundice

A

a condition caused by excess bilirubin

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43
Q

what are the symptoms of jaundice

A

skin, nail beds, whites of the eye take on a yellow color

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44
Q

What causes the excess bilirubin that leads to jaundice

A
  1. when there is too much destruction of RBCs

2. When bilirubin isn’t being secreted normally

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45
Q

when does excessive destruction of RBCs lead to excessive bilirubin levels

A

when so many RBCs are being destroyed that bilirubin levels are increasing faster than the liver is able to conjugate it

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46
Q

What things can cause bilirubin to not be secreted normally

A
  1. reduced hepatic uptake
  2. decreased ability to conjugate
  3. bile duct obstruction
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47
Q

What disorders can cause the reduced hepatic uptake that can lead to jaundice

A

cirrhosis and hepatitis

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48
Q

What disorders can cause the decreased ability of the liver to conjugate bilirubin, which leads to jaundice

A

cirrhosis, hepatitis, and enzyme deficiencies

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49
Q

what can cause the bile duct obstruction that can lead to jaundice

A

tumors or stones

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50
Q

To which types of cells is bilirubin very toxic

A

brain cells

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51
Q

What are the treatments of jaundice

A
  1. treat the causes of the condition
  2. blood transfusion
  3. Sun
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52
Q

what two things do you look for when you are trying to determine if a patients jaundice was caused by intrahepatic obstruction or extrahepatic obstruction

A

you look for the color of the urine and the feces

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53
Q

What is the cause of extrahepatic obstructive jaundice

A

obstruction of the bile duct

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54
Q

what is the cause of intrahepatic obstructive jaundice

A

damaged hepatocytes

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55
Q

What kind of jaundice is indicated by light or clay colored feces and dark urine

A

extrahepatic obstructive jaundice

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56
Q

how does extrahepatic obstructive jaundice lead to light feces and dark urine

A

the bilirubin isn’t able to be secreted with the bile and then excreted with the feces, so the feces is light. because the bilirubin can’t leave through the bile duct it goes to the kidney and leaves in the urine causing the urine to be dark

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57
Q

what kind of jaundice is indicated by light feces and light urine

A

intrahepatic obstructive jaundice

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58
Q

how does intrahepatic obstructive jaundice lead to light feces and light urine

A

because the liver can’t conjugate bilirubin, it can’t be secreted from the liver with the bile, or to the kidneys. so it just stays in the body. The lack of bilirubin in the feces and urine lead both to being light

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59
Q

what kind of jaundice is indicated by dark feces and dark urine

A

hemolytic anemia (too many RBCs being destroyed for the liver to keep up)

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60
Q

how does hemolytic anemia lead to dark feces and dark urine

A

A LOT of bilirubin is created in hemolytic anemia and the liver converts as much of it as it can and it is excreted into the urine and feces so both are dark

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61
Q

What are the three extracorpuscular hemolytic anemias

A
  1. Microangiopathic Hemolytic Anemia
  2. Warm Autoimmune hemolytic anemia
  3. Cold autoimmune hemolytic anemia
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62
Q

What are the characteristics of microangiopathic Hemolytic anemia

A
  1. extracorpuscular
  2. physical trauma to RBCs
  3. Creates Schistocytes
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63
Q

Is microangiopathic hemolytic anemia extracorpuscular or intracorpuscular

A

extracorpuscular

64
Q

how does microangiopathic hemolytic anemia affect RBCs

A

it causes physical trauma to RBCs (breaks them into pieces)

65
Q

What are schistocytes

A

fragments of RBCs

66
Q

in what type of hemolytic anemia do you see schistocytes

A

microangiopathic hemolytic anemia

67
Q

What are the common causes of microangiopathic hemolytic anemia

A
  1. artificial heart valve
  2. malignancy
  3. obstetric complications
  4. sepsis
  5. trauma
68
Q

What are the characteristic of Warm autoimmune hemolytic anemia

A
  1. Immunoglobin G (IgG) is active at high Temp
  2. it occurs in the spleen
  3. RBCs are turned into spherocytes
  4. it is extracorpuscular
69
Q

What does intracorpuscular vs. extracorpuscular anemia refer to

A

intracorpuscular anemia is anemia caused by factors inside the RBCs
extracorpuscular anemia is anemia caused by factors outside of the RBC

70
Q

is warm autoimmune anemia intracorpuscular or extracorpuscular

A

extracorpuscular

71
Q

what is the Immunoglobin that is active in warm autoimmune hemolytic anemia

A

Immunoglobin G

72
Q

Where does warm autoimmune hemolytic anemia occur

A

in the spleen

73
Q

What happens to the RBCs in warm autoimmune hemolytic anemia

A

they lose there normal shape and become spherocytes

74
Q

What are the characteristics of Cold autoimmune hemolytic anemia

A
  1. It is extracorpuscular
  2. it is caused by Immunoglobin M (IgM) and C3b
  3. It occurs inside the blood vessels
  4. it causes agglutination of RBCs
75
Q

is Cold Autoimmune hemolytic anemia extra or intracorpuscular

A

it is extra corpuscular

76
Q

what two things cause Cold Autoimmune hemolytic anemia

A

IgM and C3b

77
Q

Where does cold autoimmune hemolytic anemia occur

A

in the blood vessels

78
Q

what does cold autoimmune hemolytic anemia cause to happen to the RBCs

A

they agglutinate (stick together)

79
Q

What are the 4 types of intracorpuscular hemolytic anemia

A
  1. Sickle Cell Anemia
  2. Thalassemia
  3. Hereditary Spherocytosis
  4. G6PDH deficiency
80
Q

What are the characteristics of sickle cell anemia

A
  1. it is intracorpuscular
  2. it causes RBCs to be misshaped, and fragile
  3. it is caused by a single amino acid substitution (VAL for Glut Acid)
  4. it is autosomal recessive
  5. it is most common in Africans
  6. causes an infarcted spleen
81
Q

is sickle cell anemia intracorpuscular or extracorpuscular

A

intracorpuscular

82
Q

what does sickle cell anemia cause to happen to RBCs

A

they become misshapen and fragile

83
Q

What are some problems associated with the shape of RBCs in sickle cell anemia

A
  1. they don’t carry as much Hemoglobin
  2. they are more fragile
  3. they can become stuck in capillaries
84
Q

what causes sickle cell anemia

A

a single amino acid substitution of VAL for Glut Acid

85
Q

is sickle cell anemia a sex-linked or autosomal disorder

86
Q

is sickle cell anemia autosomal dominant or autosomal recessive

A

autosomal recessive

87
Q

Which ethnicity is most likely to have sickle cell anemia

88
Q

What happens to the spleen in sickle cell anemia

A

it becomes infarcted

89
Q

what causes the spleen to become infarcted in sickle cell anemia

A

the sickle cell shaped RBCs get stuck in the capillaries leading into the spleen, so that nothing can enter the spleen and it becomes all small and shriveled up

90
Q

which type of anemia causes an infarcted spleen

A

sickle cell anemia

91
Q

What are the characteristics of thalassemia

A
  1. it is intracorpuscular hemolytic anemia
  2. it is caused by an inability to produce alpha and beta subunits of hemoglobin
  3. it is a hypochromic anemia
  4. it is a microcytic anemia
  5. it leads to an increase in EPO and RBC synthesis
  6. it can lead to “chipmunk” cheeks
92
Q

Is thalassemia intra or extra corpuscular

A

intracorpuscular

93
Q

what causes thalassemia

A

an inability to produce either the alpha or beta subunits of hemoglobin

94
Q

in which ethnicity is an inability to produce the alpha subunit of hemoglobin (thalassemia) most common

A

South East Asian

95
Q

in which ethnicity is an inability to produce the beta subunit of hemoglobin (thalassemia) most common

A

Mediterranian

96
Q

What happens to the RBCs in thalassemia

A

they are hypochromic and microcytic

97
Q

how does thalassemia lead to hypochromic and microcytic RBCs

A

less alpha and beta subunits of hemoglobin decreases the hemoglobin content of the RBCs = hypochromic.
less hemoglobin leads to smaller RBCs = microcytic

98
Q

Why does thalassemia lead to increased EPO

A

because the malformed hemoglobin can’t carry enough oxygen, so the body increases RBC synthesis by secreting EPO

99
Q

Why does thalassemia cause “chipmunk” cheeks

A

because the body is trying to make a lot of new RBCs so the jaw expands from excessive production of RBCs

100
Q

What are the characteristics of hereditary spherocytosis

A
  1. intracorpuscular
  2. RBCs are turned into spherocytes
  3. it is caused by a spectrin defect
  4. it can be cured by a splenectomy
  5. it can lead to splenomegaly
101
Q

Is hereditary spherocytosis intra or extracorpuscular

A

intracorpuscular

102
Q

What happens to the RBCs in hereditary spherocytosis

A

the RBCs become spherocytes

103
Q

what are spherocytes

A

RBCs that are in the shape of a ball as opposed to a biconcave disk

104
Q

what causes hereditary spherocytosis

A

a spectrin defect

105
Q

how can hereditary spherocytosis be cured

A

with a splenectomy

106
Q

What is splenomegaly

A

enlargement of the spleen

107
Q

what type of anemia results in splenomegaly

A

hereditary spherocytosis

108
Q

how does hereditary spherocytosis lead to splenomegaly

A

the spherocytes in the spleen form polymers and are unable to leave the spleen and cause it to be blocked, so more RBCs enter the spleen but can’t leave so the spleen becomes enlarged

109
Q

What are howell-jolly bodies

A

they are nuclear remnants left inside of blood cells

110
Q

what do howell-jolly bodies indicate

A

they are evidence of markedly decreased splenic function

111
Q

What are the characteristics of G6PDH deficienct anemia

A
  1. it is intracorpuscular
  2. leads to increased ROS which kill RBCs
  3. causes the development and removal of heinz cells
  4. Forms bite cells
  5. Triggered by fava beans and drugs
112
Q

Is G6PDD deficient anemia intra or extracorpuscular

A

it is intracorpuscular

113
Q

How does G6PDH deficiency lead to anemia

A

deficient G6PDH leads to an loss of glutathione. Low glutathione means that Reactive oxygen species (ROS) can’t be neutralized. Increasing levels of ROS begin to lyse RBCs

114
Q

What are heinz bodies

A

When globin in the RBCs denatures and sticks to the RBC membrane

115
Q

in which type of anemia do we see heinz bodies

A

G6PDH deficient anemia

116
Q

in which type of anemia do we see bite cells

A

G6PDH deficient anemia

117
Q

what causes bite cells to form

A

G6PDH definiency causes heinz bodies to form, thenthoe heinz bodies are removed leaving a cell that looks like it has had a bite out of it

118
Q

What things can trigger G6PDH deficiency

A

Fava beans and drugs

119
Q

What are the three reasons that can cause insufficient RBC production

A
  1. too little material
  2. too few erythroblasts
  3. not enough room
120
Q

What are the three conditions that lead to too little material that can cause insufficient RBC production

A
  1. Iron deficiency
  2. Chronic Disease
  3. Megaloblastic
121
Q

What is the condition that leads to anemia due to having too few erythroblasts

A

Aplastic anemia

122
Q

what is the condition that leads to anemia due to not having enough room in the bone to produce sufficient RBCs

A

Myelophthisic anemia

123
Q

What are the characteristics of Iron-deficient Anemia

A
  1. Causes Microcytic RBCs
  2. Causes Hypochromic RBCs
  3. Shows in indented finger nails and a glossy, smooth tongue
  4. Many Causes for low iron
124
Q

What does iron-deficiency cause to happen to the RBCs

A

They become microcytic and hypochromic

they become small and have less amounts of hemoglobin

125
Q

if you see a patient with a smooth glossy tongue, and indented finger nails, what anemia is it likely that they have

A

Iron-deficient anemia

126
Q

What are the six main causes for low Iron that can lead to iron-deficient anemia.

A
  1. Decreased Iron uptake
    • poor diet
    • poor absorption
  2. Increased Iron loss
    • GI bleeding
    • Meses
    • Hemorrage
  3. Increased Iron Requirement
    • Pregnancy
127
Q

What are the characteristics of Anemia caused by chronic disease

A
  1. caused by disrupted iron metabolism due to increased hepcidin in the liver
  2. has normochromic RBCs
  3. has normocytic RBCs
128
Q

How does Chronic disease lead to Anemia

A

Chronic disease causes an increase in hepcidin in the liver. High hepcidin levels pull iron out of the blood and hold it so it isn’t used in RBC production, leading to less RBCs overall

129
Q

what does Chronic disease cause to happen to RBCs

A

they are both normocytic, and normochromic. but There are just a lot less RBCs overall

130
Q

What are the characteristics of Megaloblastic Anemia

A
  1. Caused by reduced B12/Folate in the body
  2. causes normochromic RBCs
  3. causes Macrocytic anemia
  4. Due to inadequate absorption through insufficient Intrinsic Factor
  5. Pernicious anemia is a type of megaloblastic anemia
  6. Schilling test
  7. Hypersegmented neutrophils
131
Q

What are the RBCs like in megaloblastic anemia/pernicious anemia

A

they are normochromic and macrocytic

normal hemoglobin, but extra large

132
Q

How does lack of Folate/B12 lead to megaloblastic anemia (specifically normochromic and macrocytic RBCs)

A

Folate uses B12 to “cut” cells in half that have duplicated their cellular components. So when either B12 or Folate aren’t present then these cells that are twice the size with twice the components aren’t able to divide. So the RBCs are large with the right amount of hemoglobin for their size

133
Q

How does intrinsic factor (the lack of it) lead to megaloblastic/pernicious anemia

A

Intrinsic factor is responsible for absorbing B12. so when it is lacking, so is B12, so folate can’t divide RBCs

134
Q

What happens to neutrophils in megaloblastic/pernicious anemia

A

they become hypersegmented

135
Q

Nutritional B12 deficiency is rare, but a lack of intrinsic factor can lead to malabsorption of B12. What causes lack of intrinsic factor

A
  1. Autoimmune disease of stomach
  2. GI surgery (gastric bypass)
  3. Chronic gastritis
136
Q

What is the treament for people who suffer from megaloblastic/pernicious anemia due to lack of intrinsic factor

A

B12 injections

137
Q

What does the Schilling test look for

A

it is a test to see if a patient has pernicious anemia

138
Q

what are the steps of the schilling test

A
  1. Feed patient labeled B12
  2. Inject regular B12 (to saturate the liver so it doesn’t store any)
  3. Check for labeled B12 in urine
    • if 10% of B12 is labeled in urine = Normal
    • if less that 10% of B12 is labeled in urine = Abnormal

if first round is abnormal

  1. Feed patient labeled B12 and intrinsic factor
  2. Check urine
    • if B12 levels are normal = Pernicious anemia
    • if B12 levels are still reduced = GI pathology (not pernicious anemia)
139
Q

What are the characteristics of Aplastic anemia

A
  1. Hypoplastic (empty) bone marrow
  2. pancytopenia (decreased blood cells)
  3. normochromic RBCs
  4. normocytic RBCs
  5. Causing increased bleeding and decreased immune function
    6.
140
Q

What causes aplastic anemia

A

destruction of bone marrow and Blood stem cells

141
Q

What is pancytopenia that is seen in aplastic anemia

A

a decrease in all cellular components of blood (RBC, WBC, Platelets)

142
Q

if aplastic anemia has normochromic and normocytic RBCs. How does it cause anemia

A

a significant decrease in total number of RBCs

143
Q

What does pancytopenia (thus aplastic anemia) cause

A

increased bleeding (low platelets) and decreased immune function (low WBCs)

144
Q

What are the characteristics of Myelophthisic anemia

A
  1. caused by infiltration of bone marrow by a tumor or fibrosis
  2. possible pancytopenia
  3. normochromic RBC
  4. normocytic RBC
  5. Tear shaped RBCs
145
Q

How does infiltration of bone marrow by tumors or fibrosis cause myelophthisic anema

A

the tumor or fibrosis takes up the bone marrow space that would normally be used to produce Blood cells

146
Q

What two types of anemia can cause pancytopenia

A

Myelophthisic anemia

aplastic anemia

147
Q

What type of anemia can cause tear shaped RBCs

A

myelophthisic anemia

148
Q

Other than the fact the myelophthisic anemia can cause tear shaped RBCs, what are the RBCs like

A

they are normochromic and normocytic

149
Q

which types of anemia have RBCs that are normocytic

A
  1. anemia caused by chronic disease
  2. aplastic anemia
  3. myelophthisic anemia
  4. anemia due to blood loss
150
Q

Which types of anemia have RBCs that are microcytic

A
  1. thalassemia

2. Iron deficient anemia

151
Q

which types of anemia have RBCs that are macrocytic

A
  1. Megaloblastic/pernicious anemia
152
Q

Which types of anemia have RBCs that are hypochromic

A
  1. Thalassemia

2. Iron deficient Anemia

153
Q

which types of anemia have RBCs that are normochromic

A
  1. Chronic disease induced anemia
  2. Megaloblastic anemia
  3. aplastic anemia
  4. myelophthisic anemia
154
Q

what are the types of anemia we discussed

A
  1. Microangiopathic hemolytic anemia
  2. Hot autoimmune hemolytic anemia
  3. cold autoimmune hemolytic anemia
  4. Sickle cell anemia
  5. Thalassemia
  6. hereditary spherocytosis
  7. G6PDH deficiency
  8. Iron deficient anemia
  9. anemia of chronic disease
  10. Megaloblastic (pernicious) anemia
  11. Aplastic anemia
  12. Myelophtisic anemia
155
Q

what are the causes of aplastic anemia

A
  1. idiopathic
  2. drugs
  3. viruses
  4. pregnancy
  5. fanconi anemia

DMD 5243 (17 decks)

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