Anemia Flashcards

1
Q

What is anemia?

A

the major pathophysiological condition affecting RBCs; defined as the reduction in the total number of circulating erythrocytes or a decease in the quality or quantity of hemoglobin

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2
Q

what does a CBC do?

A

measures all RBCs & RBC characteristics

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3
Q

different types of _______ produce different CBC results

A

anemia

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4
Q

the size and color of RBCs can be defined as?

A

normocytic
microcytic
microcytic
anisocytic
poilocytic

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5
Q

What does anisocytic mean?

A

cells vary in size

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6
Q

what does poilosytic mean?

A

cells varying in shape

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7
Q

what does a mean corpuscular volume (MVC) indicate?

A

size of RBCs

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8
Q

What does a mean corpuscular hemoglobin (MCH) indicate?

A

color of RBC

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9
Q

what does a mean corpuscular hemoglobin concentration (MCHC) indicate?

A

color of RBC

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10
Q

What does hematocrit levels measure?

A

percentage of blood made up of RBCs

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11
Q

What is the average hematocrit level?

A

45%

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12
Q

What is the range for hematocrit in males?

A

45 to 52%

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13
Q

What is the range for hematocrit in females?

A

37 to 48%

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14
Q

What is hematocrit at in those with anemia?

A

around 15%

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15
Q

What is hematocrit around in those with polycythemia?

A

around 65%

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16
Q

What is included in a CBC?

A

hemoglobin
hematocrit
number of RBCs
reticulocyte count
mean corpuscular volume
mean corpuscular hemoglobin
mean corpuscular hemoglobin concentration

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17
Q

What does reticulocyte count indicate?

A

bone marrow activity

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18
Q

the dx of anemia cannot be made only looking at the ________ and _________

A

hemoglobin and hematocrit

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19
Q

What does the reticulocyte count measure?

A

number of new RBCs in the blood

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20
Q

what does the reticulocyte count tell you?

A

helps to determine whether the bone marrow is producing new RBCs at an appropriate rate

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21
Q

what does increaased reticulocyte numbers associated with anemia suggest?

A

accelerated destruction or loss of RBCs

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22
Q

what is a normal reticulocyte count?

A

appoximately 1% of total RBCs

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23
Q

What can polycythemia vera be described as?

A

the opposite of anemia

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24
Q

What labs are elevated in polycythemia vera?

A

H & H

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25
Q

What is an overabundance of RBCs referred to as?

A

polycythemia vera

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26
Q

Is the cause known in primary polycythemia?

A

no

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27
Q

What happens in primary polycythemia?

A

there is hyperproliferation of all blood cells; blood becomes viscouse

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28
Q

What is there an increased risk of in primary polycythemia?

A

thromboembolism

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29
Q

Is the cause known in secondary polycythemia?

A

yes

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30
Q

is primary or secondary polycythemia more common?

A

secondary

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31
Q

What happens in secondary polycythemia?

A

hyperproliferation of the RBCs in response to chronic blood hypoxia (like in COPD)

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32
Q

about 98% of all cases of polycythemia are related to a mutation in the ____ gene

A

JAK2

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33
Q

polycythemia causes RBC crowding which may cause an increased risk of ______, ______, & increased risk of _______ due to blood escaping the vessel.

A

clots; brusing; bleeding

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34
Q

What is one way that polycythemia can be treated?

A

therapeutic phlebotomy; taking blood out of the body

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35
Q

What lab testing can be done to diagnose anemia?

A
  • CBC
  • peripheral blood smear
  • iron
  • folic acid
  • bone marrow aspiration and/or biopsy
  • additional test based on type of anemia
  • fecal occult blood test
  • vitamin B12 levels
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36
Q

What other testing can be done to help diagnose anemia?

A
  • echocardiogram
  • electrocardiogram(EEG)
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37
Q

What are the 3 major causes of anemia?

A
  • decreased erythrocyte production
  • increased erythrocyte destruction
  • blood loss
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38
Q

Can you have more than one cause of anemia?

A

yes; can have a combination of any of the 3 causes

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39
Q

What are the 4 classic S & S of anemia?

A
  • pallor
  • fatigue
  • dyspnea on exertion
  • dizziness
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40
Q

What are compensatory mechanisms that are manifestations of anemia?

A
  • tachycardia
  • palpitations
  • vasoconstriction
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41
Q

What are respiratory manifestations of anemia?

A
  • tachypnea
  • increased depth
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42
Q

What are other manifestations of anemia?

A
  • increased interstitial fluid into vascular space
  • cold hands/feet
  • chest pain
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43
Q

how much blood can an adult lose without serious or lasting effects?

A

500ml

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44
Q

What can happen if blood loss reaches 1000ml or more?

A

serious adverse effects like hypovolemia shock & cerebral hypoperfusion

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45
Q

What is acute blood loss?

A

a rapid ;loss of blood as in hemorrhage

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46
Q

What can cause acute blood loss?

A
  • trauma
  • childbirth
  • rupture of a major blood vessel or organ
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47
Q

in what disorders can severe GI bleeding occur?

A
  • esophageal varices
  • penetrating peptic ulcers
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48
Q

What do those with bleeding due to esophageal varices often exhibit?

A

hematoemesis

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49
Q

What is coffee ground emesis?

A

blood mixed with stomach acid & mucus in vomit

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50
Q

What is melena?

A

blood mixed in stool causing dark, tarry stool

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51
Q

What is hematoachezia?

A

bright red blood in stool

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52
Q

What are the most common causes of anemia due to chronic blood loss?

A
  • peptic ulcers
  • Inflammatory bowel disease
  • colon cancer
  • menorrhagia (heavy or prolonged menstrual cycles)
  • chrones
  • ulcerative colitis
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53
Q

What is the most common type of anemia?

A

iron deficiency anemia

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54
Q

in what gender is iron deficiency anemia more common?

A

females

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55
Q

iron deficiency anemia is _______- ________

A

microcytic- hypochromic

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56
Q

What are the 8 possible causes of iron deficiency anemia?

A
  • poor dietary intake
  • menses
  • pregnancy
  • ulcerative colitis
  • certain medications
  • parasitic infections
  • neoplasms
  • can also occur in lead poisoning
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57
Q

What is the main nutritional element needed for hemoglobin sythesis?

A

iron

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58
Q

What is iron composed of?

A

a heme & globin compound

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59
Q

balance is maintained between iron used as __________ and iron placed in ________

A

hemoglobin; storage

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60
Q

Can iron be recycled?

A

yes

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61
Q

iron is in ________ demand

A

constant

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62
Q

How many grams of iron is in the body at all times?

A

3-4

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63
Q

How much of iron is held in hemoglobin?

A

60%

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64
Q

how much iron is stored as ferritin in the macrophages, liver, spleen, and bone marrow?

A

35%

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65
Q

What is the rest of iron found in?

A

in myoglobin and bound to transferrin

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66
Q

why is there very little free iron?

A

it it toxic to the cells

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67
Q

What does serum iron test for?

A

the level of circulating iron in the blood; % saturated

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68
Q

What is TIBC?

A

total iron binding capacity; percentage of cells that are actually filled with transferrin

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69
Q

What is the normal serum iron level?

A

25 -45%

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70
Q

What is the serum iron in those with iron deficient anemia?

A

less than 20%

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71
Q

What is ferritin?

A

protein for iron stores (like a bank or pantry)

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72
Q

What is happening in iron deficient anemia?

A
  • pt is using more iron than what is being saved so pt needs to go to stores
  • iron needs exceed intake & stores are depleted
  • there are no stores & daily intake is not adequate to maintain hemoglobin levels
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73
Q

How do iron deficiency anemia symptoms usually come on?

A

onset of sx are gradual & appear at different times based on the individual

74
Q

when may some people begin to experience sx?

A

when hemoglobin is around 7-8 g/dl

75
Q

What are some manifestations of iron deficiency anemia?

A
  • non-specific sx
  • pica
  • epithelial tissue damage occurs
  • koilonychia
  • pallor of conjunctiva
76
Q

What is koilonychia?

A

the “spooning” of the nail bed

77
Q

What do you check to dx iron deficient anemia?

A
  • hemoglobin
  • MCV/MCH/MCHC
  • bone marrow biopsy/aspirate
    serum iron profile
  • iron
  • TIBC
  • transferrrin
  • ferritin
78
Q

what lab may be affected initially in iron deficient anemia?

79
Q

What may the MCV, MCH, & MCHC results be in iron deficient anemia?

A

MCV will be low (less than 80)
MCH/MCHC will also be low

80
Q

How can you treat iron deficient anemia?

A
  • iron salts: ferrous sulfate, ferrous gluconate
  • orange juice to improve absorption
  • carbonyl iron: pure elemental iron
  • IV iron: dextran
81
Q

What is the most common oral form of iron used?

A

ferrous sulfate

82
Q

How much elemental ron does ferrous sulfate contain?

83
Q

What are the side effects of ferrous sulfate?

A
  • nausea
  • heartburn
  • constipation!
  • black/dark green stool
  • teeth staining
84
Q

should you take ferrous sulfate with or without food?

85
Q

how can you help mitigate teeth staining when taking ferrous sulfate?

A

dilute in juice or other beverage
drink with straw
rinse mouth afterward

86
Q

what should you avoid when taking ferrous sulfate?

A

avoid coffee, tea, soda, and all calcium-containing foods

87
Q

concurrent administration of ferrous sulfate with antacids or tetracycline (increases/decreases) absorption

88
Q

PPl and H2 blockers (decrease/increase) ferrous sulfate absorption

89
Q

while slow-release ferrous sulfate is easier on the stomach, it is less effective. Why is that?

A

the acid in the duodenum protects the iron but the HCO3 from the pancreas can destroy it

90
Q

What are the two options for IV iron?

A
  • low molecular weight iron dextran
  • ferric gluconate
91
Q

how is IV ferric gluconate administered?

A

diluted in NNS & infused over 20-60 minutes depending on dose

92
Q

What is done before a full dose of ferric gluconate is given?

A

a test dose (over 5 min) to be sure there is no reaction

93
Q

What can ferric gluconate cause?

A

can cause prodromal sx & if bad, infusion is stopped & then often resumed

94
Q

What are indications to receive IV iron?

A
  • abnormal uterine bleeding
  • postpartum
  • inflammatory bowel disease
  • chronic kidney disease
95
Q

What are adverse effects that may occur with IV iron?

A
  • hypotension
  • anaphylaxis (triggered by dextran): less incidence with other forms of IV iron
96
Q

What is the cause of megaloblastic anemia?

A

due to impaired DNA synthesis that causes ineffective erythropoiesis
- results in large stem cells that mature into large but fragile erythrocytes
- defective cells dying too early which decreases numbers in the circulation

97
Q

What are CBC characteristic in megaloblastic anemia?

A
  • anemia
  • macrocytic
  • normo or hyperchromic
98
Q

What is megaloblastic anemia usually related to?

A

deficiencies in vitamin B12 & folic acid

99
Q

When do megaloblastic anemia sx usually present?

A

when advanced, megaloblastic anemia has a slow progession

100
Q

What is pernicious anemia a deficiency in?

A

vitamin B12

101
Q

pernicious anemia is ____ if left untreated

102
Q

why is pernicious anemia rare in the US?

A

vitamin B12 comes from animal products, milk & eggs

103
Q

What is pernicious anemia thought to be?

A

an autoimmune disorder

104
Q

What causes pernicious anemia?

A
  • conditions that cause malabsorption of B12
  • decreased intake of B12 products (vegans)
  • defective gastric secretions of intrinsic factor from parietal cells of the gastric mucousa
  • excessive alcohol use
105
Q

B12 is needed for ____ ______ and nuclear maturity

A

DNA synthesis

106
Q

What prevents abnormal fatty acids from affecting neural lipids which could result in myelin breakdown?

107
Q

Where does B12 come from?

A

animal sources

108
Q

What does B12 bind to?

A

binds to intrinsic factor which is made from parietal cells in the stomach

109
Q

What is necessary for B12 absorption?

A

intrinsic factor

110
Q

Where is B12 released from intrinsic factor and crosses over to the blood stream?

111
Q

What does B12 bind to that takes it to the storage sites?

A

transcobalamin

112
Q

What does type A chronic gastritis do?

A

destroys all cells that produce secretions in the stomach; affects B12 absorption

113
Q

how do proton pump inhibitors affect vitamin B12?

A

decrease absorption; decrease in HCL-HCL needed for absorption

114
Q

What are things that reduce or eliminate B12 absorption?

A
  • anything that affects parietal cells
  • autoimmune disorders or genetic changes
    -H pylori infections
  • excessive ETOH
  • smoking
  • hot tea ingestion
  • gastrectomy
  • gastric bypass
115
Q

What are the clinical manifestations of pernicious anemia?

A
  • classic S & S of anemia
  • slow development so sx appear in advanced disease
  • fatigue; mood swings
  • anorexia; weight loss
  • hyperbilirubinemia
  • hepatosplenomegaly (in severe cases)
116
Q

What are the neurologic sx with severe anemia (hbg <7)?

A
  • parethesia of hands & fingers
  • ataxia
  • memory loss
  • vision changes
  • weakness, clumsiness, & an unsteady gait
  • loss of proprioception
117
Q

how can pernicious anemia be dx?

A

CBC w diff
- low H & H
- MCV will be >100
- MCHC/ MHC will be normal
vitamin B12 levels
intrinsic factor
antibodies to parietal cells & IF will be found
bone marrow aspiration

118
Q

How do you tx pernicious anemia?

A

vitamin B12
oral, if deficiency is not the problem
- prefered route
injection, if deficiency is the problem
- can be SQ, IM, or intranasal

119
Q

How do you know treatment for pernicious anemia is working?

A

will know treatment working by rising reticulocyte count and should normalize in 6 weeks

120
Q

What kind of anemia is caused by folic acid deficiency?

A

megaloblastic anemia (macrocytic & normochromic)

121
Q

What is folic acid needed for?

A

DNA synthesis & red cell maturation (thymine & adenine)

122
Q

is folic acid or B12 deficiency more common?

A

folic acid

123
Q

What does folic acid deficiency lead to?

A

large ineffective RBC

124
Q

In what foods is folic acid found?

A
  • vegetables
  • fruits
  • cereals
  • meat (lost in cooking)
125
Q

How much folic acid is stored in the body?

A

500-20,000 mcg

126
Q

How much folic acid is needed per day?

A

50-100 mcg/day

127
Q

how quickly does dietary deficiency of folic acid result in anemia?

A

within a few months

128
Q

Who are at risk for folic acid deficiency?

A
  • pregnant & lactating women
  • alcoholics
  • fad diets
  • individuals with celiacs or IBS
  • those with chronic inflammatory disorders
129
Q

Why are pregnant/ lactating women at risk for folic acid deficiency?

A

need increaes 5-10x. folic acid is needed for neural tube development

130
Q

Why are alcoholics at risk for folic acid deficiency?

A

interferes with folate metabolism

131
Q

why are those on fad diets at increased risk for folic acid deficiency?

A

decrease folate intake

132
Q

What kind of chronic inflammatory diseases can result in folic acid deficiency?

A
  • rheumatoid arthritis
  • tuberculosis
  • psoriasis
  • bacterial endocarditis
  • systemic infections
133
Q

What are clinical manifestations are seen in megaloblastic anemia related to folic acid?

A

classic S&S of anemia
no neurologic sx
manifestations r/t malnourishment
- cheilosis
- stomatitis
- burning mouth syndrome
- dysphagia
- flatulence
- GI disturbances
undiagnosed IBD

134
Q

how is folic acid deficiency diagnosed?

A

CBC
- changes in indices before hemoglobin
- MCV> 100
- MCHC & MHC normal
folic acid levels will be low

135
Q

What is required for folic acid to be converted to active form?

136
Q

What are the two forms of folic acid that can be given?

A

active
inactive

137
Q

is active or inactive folic acid more commonly given?

138
Q

how can inactive folic acid be given?

A

folate (oral)
can be PO, IV, SQ, IM
treat with supplementation

139
Q

What should you be monitoring when treating folic acid deficiency?

A

hemoglobin & reticulocyte count

140
Q

What does aplastic anemia result from?

A
  • breakdown in production in bone marrow stem cells that inhibit growth of RBC, WBC, & platelets
  • a failure of the marrow to replace the senescent red cells as they are destroyed & leave the circulation
141
Q

What is the cell size and color like in aplastic anemia?

A

normal size & normal color

142
Q

What does aplastic anemia usually present as?

A

infection or bleeding

143
Q

Why does aplastic anemia present as infection or bleeding opposed to anemia?

A

since WBC & platelets have a shorter life span

144
Q

What is the onset of aplastic anemia usually like?

A

can be abrupt or gradual

145
Q

What are causes of aplastic anemia?

A
  • radiation exposure
  • chemotherapy: inhibits hematopoiesis
  • chemicals: benzene
  • viral illness such as hepatitis, mono, HIV
  • pregnancy
    cytokines suppress normal stem cell development
146
Q

cause of aplastic anemia is unknown in about _____ of cases

147
Q

How is aplastic anemia dx?

A

CBC shows pancytopenia
WBC count <200: increasing risk for opportunistic infections
RBC: normocytic & normochromic

148
Q

How do you treat aplastic anemia?

A

treat the cause

149
Q

What may be needed to treat aplastic anemia?

A

BM transplant
immunosuppressive therapy
prophylactic antibiotics
platelet, RBC, or WBC transfusions

150
Q

What are symptoms of aplastic anemia?

A
  • infection
  • present with fatigue, weakness, pallor
  • petechiae/purpura
  • ecchymosis
  • bleeding from body orifices
151
Q

who are the ideal donors for bone marrow transplants?

152
Q

What are the two bone marrow stimulants that can be used to treat aplastic anemia?

A

filgrastim (Neupogen)
epoetin-alfa (epogen)

153
Q

How long do bone marrow stimulants take to work?

A

about a month

154
Q

What are the 4 ways hemolytic anemia is aquired?

A
  • drug reactions
  • infections
  • transfusion reactions
  • ABO or Rh factor incompatibility of mother or fetus
  • autoimmune disease
155
Q

What is hemolytic anemia cause by?

A

premature or accelerated destruction of RBCs

156
Q

What are the inherited forms of hemolytic anemia?

A

structure deficits
enzyme deficiencies
defects in globin synthesis or stucture
- sickle cell
- thalassemia

157
Q

How many people are affected by sickle cell in the US?

158
Q

What ethnicities have the highest concentration of sickle cell?

A

black people, middle eastern people, and Mediterranean people

159
Q

How many births result in sickle cell?

A

1: 400-500

160
Q

What is the cause of sickle cell?

A

inherited defect of hemoglobin S leads to hemolytic anemia & chronic organ damage

161
Q

if someone has a defective sickle cell gene from 1 parent what are they considered?

A

a carrier; they do not have sickle cell

162
Q

What must happen for someone to have sickle cell anemia?

A

must inherit the defective gene from both parents

163
Q

sickle cell usually causes little problem when properly ___________

A

oxygenated

164
Q

What happens when oxygen drops in sickle cell?

A

fluid polymers realign and cause cells to sickle

165
Q

What does sickle cell depend on?

A
  • hydration
  • PH
  • oxygenation
166
Q

What do sickled cells do?

A

plug the blood vessels; increase the viscosity

167
Q

What can sickled cells lead to?

A
  • occlusion of the vessels
  • pain
  • infarction
  • pool in the spleen and hemolysis & can infarct vessels in the spleen
168
Q

Sickling is not always _________ as the other chains are normal and will produce ___________ ___

A

permanent; hemoglobin A

169
Q

When do sickled cells return to normal?

A

after rehydration & oxygenation

170
Q

What happens if plasma membrane damage occurs in sickle cell?

A

cell is irreversibly sickled

171
Q

The higher the number of cells with hgb S the higher the risk for ___________ sickling - up to even __%

A

irreversible; 30%

172
Q

do people with the sickle cell trait experience sx?

173
Q

Are infants affected by sickle cell anemia?

A

infants are initially okay because the primary component of their hemoglobin is Hgb F. it takes a few months for hbg S to take over

174
Q

What are the three main crisis’ that result from sickle cell?

A

vaso-occlusive crisis
sequestration crisis
aplastic crisis

175
Q

What happens during a vaso-occlusive crisis?

A
  • sickling in microcirculation
  • obstruction of blood flow
  • creates a log jam; no blood can move through the vessel
176
Q

what can a vaso-occlusive crisis cause?

A

severe pain
can lead to CVA or MI

177
Q

How long can a vaso-occlusive crisis last?

A

days to weeks

178
Q

What happens during a sequestration crisis?

A
  • large amounts of blood pool in the liver & spleen
  • causes CV collapse as 20% of blood can pool in the liver/spleen
179
Q

in what age group do sequestration crisis’ occur?

A

small children

180
Q

what is an aplastic crisis?

A
  • extreme anemia from decreased RBC count
  • sickled RBC only lives for 10-20 days
  • compensatory mechanism in place but if dysfunctional aplastic anemia occurs
181
Q

How is sickle cell dx?

A
  • mandatory screening at birth using electrophoresis which identified the HB F from the hb A and hbS
  • mandatory screening in college athletes NCAA regulations
182
Q

How can you treat sickle cell?

A
  • prevent complications & crisis
  • hydroxyurea: produces more hbF & therefore displaces the hbS
  • anticoagulants
  • decrease inflammatory response
  • pain management