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NUR516 > Anemia > Flashcards

Anemia Flashcards

1
Q

Anemia is major ______ condition affecting _____

A

Pathophysiological; RBCs

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2
Q

Anemia defined as

A

Reduction in the total # of circulating erythrocytes or a decrease in quality or quantity of Hgb

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3
Q

What does a CBC measure?

A

All RBCs & RBC characteristics
Diff types of anemia produce diff CBC results

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4
Q

Classification of anemias:

Morphology

A

Size → normo, micro, or macrocytic
Color → normo, hypo, or hyper
other:
- Anisocytic
- Poikilocytosis

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5
Q

Anisocytic is defined as

A

Varying sizes

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6
Q

Poikilocytosis is defined as

A

Varying shapes

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7
Q

Classification of anemias

Measures of morphology

A

Mean corpuscular volume (MCV)
Mean corpuscular Hgb (MCH)
Mean corpuscular Hgb concentration (MCHC)

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8
Q

Normal Hematocrit levels

A

Normal: 45%
-Males → 45 - 52%
-Females → 37 - 48%

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9
Q

Hematocrit levels in someone with anemia?

A

15%

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10
Q

Hematocrit levels in someone with polycythemia?

A

~ 65%

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11
Q

What does Reticulocyte count indicate?

A

Bone marrow activity

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12
Q

What indicates size of RBCs?

A

Mean corpuscular volume (MCV)

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13
Q

What indicates color of RBCs?

A

Mean corpuscular Hgb (MCH)
Mean corpuscular Hgb concentration (MCHC)

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14
Q

Solely looking at Hgb & Hct levels cannot ….

A

Make the Dx of anemia!!

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15
Q

RBC → size & color normal & abnormal ranges of MCV & MCHC

A

Normal → MCV 80-100
Microcytic → MCV < 80
Macrocytic → MCV > 100
Hypochromic → MCHC low

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16
Q

What does reticulocyte count measure?

A

Number of new RBCs in the blood & helps to determine whether the BM is producing new RBCs at an appropriate rate

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17
Q

Increased reticulocyte is associated with anemia suggesting

A

accelerated destruction or loss of RBCs

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18
Q

What % of total RBCs is a normal reticulocyte count

A

~ 1%

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19
Q

Polycythemia vera

A

Opposite of anemia
Elevated Hct & Hgb levels
Overabundance of RBCs in polycythemia

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20
Q

Primary polycyhtemia

A

Unknown cause
Hyperproliferation of ALL blood cells
-Blood becomes viscous which can ↑ risk of thromboembolisms

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21
Q

Secondary polycythemia

A

Known cause
More common & a hyperproliferation of RBCs in response to chronic blood hypoxia (i.e COPD)

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22
Q

~ 98% of all polycythemia cases are related to …

A

a mutation in the JAK2 gene

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23
Q

Lab studies to Dx anemia

A

CBC
Peripheral blood smear
Iron
Folic acid
BM aspiration &/or biopsy

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24
Q

Diagnostic studies to Dx anemia

A

Echocardiogram
Electrocardiogram (ECG)

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25
Q

Additional diagnostic tests based on type of anemia

A

Fecal occult blood test
Vitamin B12 level

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26
Q

List 3 causes of anemia

A
  1. ↓ erythrocyte production
  2. ↑ erythrocyte destruction
  3. blood loss
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27
Q

Classic S/S of anemia

A

Pallor
Fatigue
Dyspnea on exertion
Dizziness

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28
Q

Compensatory mechanisms of anemia

A

Tachycardia
Palpitation
Vasoconstriction

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29
Q

Respiratory clinical manifestations of anemia

A

Tachypnea
Increased depth on respirations

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30
Q

Other clinical manifestation Sx of anemia

A
  1. ↑ interstitial fluid into vascular space
  2. cold hands & feet
  3. chest pain
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31
Q

How much blood could an adult lose w/o severe or lasting effects?

A

500 mL

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32
Q

Blood losses of 1000mL or more can have serious adverse effects such as:

A

Hypovolemic shock
Cerebral hypoperfusion

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33
Q

Acute blood loss (anemia)

A

Rapid loss of blood (hemorrhage) caused by trauma, childbirth, rupture of major BV or organ

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34
Q

Severe GI bleeding can occur in what disorders?

A

Esophageal varices
Penetrating peptic ulcer

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35
Q

Pathophysiology of acute blood loss

A

Hypoxia develops → kidneys produce eryhtropoietin → BM starts to synthesize RBCs → Hypovolemia →RAAS activated (releases ADH)

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36
Q

Pathophys of acute blood loss:

When experiencing hypovolemia

A

Baroreceptors sense a decrease in BP which signals the SNS (increases activity) for the arteries to vasoconstrict in an attempt to ↑ BP

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37
Q

Subjective S/S for pt with:

Reduced O2 carrying capacity leading to hypoxia of tissues:

A

Fatigue
Bone pain from erythropoiesis
Angina
Dyspnea
↑ RR to ↑ O2 to tissues
Weakness

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38
Q

Objective S/S of pt with:

Reduced O2 carrying capacity leading to hypoxia of tissues:

A

Tachycardia/ palpitations
Flow heart murmur
Pallor of skin & mucus membranes
> 40% total volume results in profound shock

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39
Q

Blood loss from GI tract:

Pts bleeding b/c of esophageal varices often exhibit _____

A

Hematemesis

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40
Q

Blood loss form GI tract:

____ _____ ____ is blood mixed with stomach acid & mucus in vomitus

A

Coffee ground emesis

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41
Q

Blood loss from GI tract:

_____ is blood mixed in stool, causing dark, tarry stool

A

Melena

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42
Q

Blood loss from GI tract:

______ → bright red blood in the stool

A

Hematochezia

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43
Q

Most common causes of Anemia from chronic (slow) blood loss

A

Peptic ulcer
Inflammatory bowel disease
Colon cancer
Menorrhagia

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44
Q

What is menorrhagia?

A

excessive monthly menstrual loss

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45
Q

What is the most common type of Anemia?

A

Iron deficiency anemia

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46
Q

Iron deficiency anemia RBC characterisitcs

A

Microcytic-hypochromic

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47
Q

Iron deficiency anemia is more common in ____

A

females

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48
Q

List the causes of Iron deficiency anemia

A

Poor dietary intake
Menses
Pregnancy
Ulcerative colitis
Certain medication
Parasitic infections
Neoplasms
Possibly from lead poisoning

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49
Q

Iron is the main nutritional element needed for ____ ____

A

Hgb synthesis

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50
Q

How many grams of iron are in the body at any given time?

A

3-4 grams
-60% of iron held in Hgb (RBCs)
-35% stored as ferritin in macrophages, liver, spleen, BM
-Rest in myoglobin & bound to transferrin (protein)

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51
Q

Why is there very little free iron in the body?

A

Toxic to the cells

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52
Q

Iron studies:

Serum iron

A

Level of circulating iron in the blood
% saturated
-TIBC → % of cells filled w/ transferrin
-Normal → 25-45%
-Iron deficient anemia → < 20%

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53
Q

Iron studies:

Ferritin

A

Protein for iron stores
Like a bank or pantry

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54
Q

What happens in iron deficient anemia

A

Using more Fe than what is being saved & need to go to stores
-Needs exceed intake & stores are depleted
-No stores & daily intake is NOT enough to maintain Hgb levels

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55
Q

Stage 1 iron deficiency anemia

A

Iron stores for RBC & Hgb synthesis are depleted
-Normocytic/ Normochromic
-Ferritin levels will start to drop

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56
Q

Stage 2 iron deficiency anemia

A

Insufficient levels of iron are taken to the marrow
-Iron deficient RBC production begins
-Cells will begin to ↓ in size & become pale

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57
Q

Stage 3 iron deficiency anemia

A

Hgb deficient cells enter the circulation & replace the dying RBC
-Hgb begins to drop
-Microcytic/ Hypochromic

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58
Q

Clinical manifestations of iron deficiency anemia

A

Onset of Sx gradual & appear at diff times per person
-Some may not experience Sx until 7-8 g/dL
-Non-specific Sx
-PICA
As it progresses, epithelial tissue damage occurs

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59
Q

Epithelial tissue damage in IDA can lead to

A

Koilonychia → sunken nails
Pallor of conjuctiva

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60
Q

Dx of iron deficient anemia

A

Check Hgb
Check MCV, MCH, MCHC
Serum iron profile
-Iron; TIBC; Tranferrin; Ferritin
BM biopsy/ aspirate

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61
Q

Dx of iron deficient anemia

Initially (esp. in chronic slow bleed) what may be the only thing affected?

A

Ferritin & as it continues the indices, Hgb will be affected

62
Q

Dx of iron deficient anemia

MCV levels

63
Q

Dx of iron deficient anemia

MCH/ MCHC levels

64
Q

Tx of iron deficiency anemia

A

Oral iron
-Iron salts
-Orange juice
-Carbonyl iron
-IV iron → dextran

65
Q

Give examples of iron salts

A

Ferrous sulfate; ferrous gluconate

66
Q

Why is orange juice used to Tx IDA

A

improves absorption

67
Q

What kind of iron is carbonyl iron?

A

Pure elemental iron

68
Q

What is the most common oral form of iron?

A

Ferrous sulfate → contains 65 mg of elemental iron

69
Q

Side effects of ferrous sulfate

A

GI (Nausea; Heartburn; Constipation)
-Take with food
-makes stool black/ dark green
Teeth staining
-Dilute in juice, drink w/ straw, rinse mouth after

70
Q

Precautions with using ferrous sulfate

A

Avoid w/ coffee, tea, soda & calcium containing foods
Admin with antacids/ tetracyclines ↓ absorption

71
Q

What type of ferrous sulfate may be easier on the stomach but less effective?

A

Slow release → less effective as the acid in duodenum protects the iron but the HCO3 from the pancreas can destroy

72
Q

_____ & _____ blockers will ↓ absorption of ferrous sulfate

73
Q

IV iron

A

Low molecular weight iron dextran or ferric gluconate

74
Q

Ferric gluconate

A

Diluted in NSS & infused over 20-60 min
-Test dose (over 5 min) ensure no reaction

75
Q

What can ferric gluconate cause & what is done with infusion?

A

Can cause prodromal Sx & if bad infusion is stopped & then resumed

76
Q

When is ferric gluconate often used?

A

Abnormal uterine bleeding
Post partum
Inflammatory bowel disease
CKD

77
Q

Adverse effects of IV irons

A

Hypotension
Anaphylaxis (Dextran)
-less incidence w/ other IV iron forms

78
Q

Megaloblastic anemia occurs from

A

Impaired DNA synthesis that causes ineffective erythropoiesis

79
Q

Megaloblastic anemia results in

A

Large stem cells that mature into large but fragile erythrocytes
-defective cells dying too early which ↓ #s in circulation (eryptosis)

80
Q

CBC characteristics of megaloblastic anemia

A

Anemia
Macrocytic
Normo- or hyperchromic

81
Q

Megaloblastic anemia related to what two deficiencies

A

Vitamin B12
Folic acid

82
Q

What type of progression is megaloblastic anemia?

A

Slow progression so Sx only present when advanced

83
Q

Pernicious anemia

A

AKA: deficiency in vitamin B12
Fatal is left untreated
thought to be autoimmune disorder

84
Q

Causes of pernicious anemia

A

Conditions that cause malabsorption of B12
↓ intake of B12 products (vegans)
defective gastric secretions of intrinsic factor from parietal cells of gastric mucosa

85
Q

Vitamin B12 is needed for _____ synthesis & _____ maturity

A

DNA synthesis & nuclear maturity

86
Q

Vitamin B12 prevents

A

abnormal fatty acids from affecting neural lipids which can result in myelin breakdown

87
Q

Where does vitamin B12 come from?

A

animal source & binds to intrinsic factor → made from parietal cells in stomach

88
Q

What is necessary for vitamin B12 to be absorbed?

A

Intrinsic factor

89
Q

Where does intrinsic factor take the vitamin B12?

A

Takes to ileum where it is released from intrinsic factor & crosses over to blood stream

90
Q

What does vitamin B12 bind to in the bloodstream?

A

Binds to transcobalamin II which takes it to the storage sites

91
Q

Pernicious anemia has a ____ development so Sx appear in _____ disease

A

Slow development; Advanced disease

92
Q

Pernicious anemia usually has vague signs such as

A

fatigue
mood swings

93
Q

Sx of pernicious anemia

A

Anorexia
weight loss
hyperbilirubinemia
Neurologic (severe)
Hepatosplenomegaly (severe)

94
Q

When could neuro Sx occur in pernicious anemia?

A

when Hgb < 7 g/dL

95
Q

List neuro Sx of pernicious anemia

A

Paresthesia of hands & fingers
Ataxia
Memory loss
Vision changes
Weakness, clumsiness, & an unsteady gait
Loss of proprioception

96
Q

Pernicious Anemia is NOT just about IF also from anything that ↓ or eliminates B12 including:

A

Type A chronic gastritis → destroys all cells that create secretions in stomach
Anything that affects parietal cells
Autoimmune diseases/ Genetic changes
? H. Pylori infection
Excessive ETOH, smoking, or hot tea ingestion
Gastrectomy or Gastric bypass
PPI will ↓ B12 absorption → ↓ in HCl which we need for absorption

97
Q

Diagnosis of Pernicious anemia

A

CBC with differential
Vitamin B12 levels
Intrinsic factor
Ab to parietal cells & IF will be found
Bone marrow aspiration

98
Q

Diagnosis of Pernicious anemia

What will you see on CBC w/ differential

A

Possible low H & H
MCV > 100
MCHC / MHC → normal

99
Q

Tx of pernicious anemia

A

Vitamin B12 → cobalamin or cyanocobalamin
Oral (if deficiency isn’t problem)
-Preferred route
Injection (if deficiency is problem)
-Can be SQ, IM, intranasal

100
Q

How will we know if Tx is working in pt with pernicious anemia?

A

By rising reticulocyte count & should normalize in 6 wks

101
Q

What do we need folic acid for?

A

DNA synthesis & red cell maturation (thymine & adenine)

102
Q

Folic acid deficiency anemia

A

Type of megaloblastic anemia (macrocytic & normochromic)

103
Q

Is folic acid deficiency anemia more or less common than vitamin B12 deficiency?

A

More common

104
Q

Folic acid deficiency leads to _____ _____ RBCs

A

Large ineffective RBCs

105
Q

Where can folic acid be found?

A

Vegetables
Fruits
Cereals
Meat (but lost in cooking)

106
Q

How much folic acid does the body store?

A

500-20,000 mcg & needs 50-100 mcg/day

107
Q

When will anemia occur from folic acid dietary deficiency?

A

Within a few months

108
Q

Who is at risk for folic acid deficiency?

A

Pregnancy & lactation
Alcoholics
Fad diets
Individuals w/ celiac or inflammatory bowel disease
Chronic inflammatory disorders

109
Q

Why are pregnant & lactating clients at ↑ risk for folic acid deficiency?

A

Their needs increase 5-10x
-Needed for neural tube development so supplement very important

110
Q

Why are alcoholics at ↑ risk for folic acid deficiency?

A

Interferes with folate metabolism

111
Q

Why are people who follow fad diets at ↑ risk for folic acid deficiency?

A

Decreased folate intake

112
Q

What types of chronic inflammatory disorders have ↑ risk for folic acid deficiency?

A

rheumatoid arthritis
tuberculosis
psoriasis
bacterial endocarditis
systemic infections

113
Q

Clinical manifestations of Folic acid deficiency

A

Classic signs of anemia
No neuro Sx
Manifestations r/t malnourishment
undiagnosed IBD

114
Q

List some manifestations r/t to malnourishment in folic acid deficiency

A

Cheilosis
Stomatitis
Burning mouth syndrome
Dysphagia
Flatulence
GI disturbances

115
Q

Diagnosis of Folic acid deficiency:

CBC

A

Will see changes in indices before Hgb
MCV > 100
MCHC & MHC → normal

116
Q

Diagnosis of Folic acid deficiency:

What levels will be low?

A

Folic acid levels

117
Q

Tx of folic acid deficiency:

Folic acid requires ____ to be converted to ____ ____

A

B12; active form

118
Q

Tx of folic acid deficiency:

Two forms:

A

Active & Inactive

119
Q

Which form of folic acid is more common for Tx of folic acid deficiency?

120
Q

Inactive form of folic acid

A

Folate
Can be given PO, IV, SQ, IM
Tx with supplementation

121
Q

What labs are important to monitor for a pt w/ folic acid deficiency?

A

Hgb & reticulocyte count

122
Q

Aplastic Anemia Results from …

A

Breakdown in production in BM stem cells that inhibit growth of RBC, WBC, & PLTs

123
Q

Aplastic anemia results as failure of the _____ to replace the ____ red cells as they are destroyed & leave the _____

A

Marrow; senescent; circulation

124
Q

Characteristics of RBCs in Aplastic anemia

A

Cells are normal size & color

125
Q

What happens in Aplastic anemia due to WBCs & PLTs having shorter life spans?

A

The disease often presents with infection or bleeding

126
Q

Describe onset of aplastic anemia

A

Can be either abrupt or gradual

127
Q

Causes of Aplastic Anemia

A

Radiation exposure
Chemo → inhibits hematopoiesis
Chemicals → Benzene
Viral illness (Hepatitis, mono, HIV)
Pregnancy
Unknown → ~ 2/3 cases
Cytokines suppress normal stem cell development

128
Q

Diagnosis of Aplastic Anemia

A

CBC → shows pancytopenia
-WBCs → < 200/mm3 (↑ risk of opportunistic infections)
-RBCs → normocytic/ normochromic

129
Q

Symptoms of Aplastic Anemia

A

Infection
Fatigue, pallor, weakness
Petechiae/ Purpura
Ecchymosis
Bleeding from body orifices

130
Q

Tx of Aplastic Anemia

A

Treat underlying cause
BM transplant from sibling donor → preferred Tx
Prophylactic Abx & PLT, RBC, & WBC transfusions may be required
BM Stimulants

131
Q

Tx of Aplastic Anemia:

List two bone marrow stimulants

A

Filgrastim (NeupogenR)
Epoetin-alfa (EpogenR)

132
Q

Hemolytic anemia can be ____ or ____

A

Acquired or Hereditary

133
Q

Acquired hemolytic anemia results from

A
  1. Drug reactions
  2. Infections
  3. Transfusion reactions
  4. ABO or Rh incompatibility of mom & fetus
  5. Autoimmune diseases
    Caused by premature, accelerated, or destruction of RBCs
134
Q

Hereditary hemolytic anemia results from

A

Structure deficits
Enzyme deficiencies
Defects in globin synthesis or structure
-Sickle cell
-Thalassemia

135
Q

Sickle cell anemia has highest concentration in

A

African Americans, Middle East, & Mediterranean countries

136
Q

What is sickle cell anemia?

A

Inherited defect of Hgb S → leads to hemolytic anemia & chronic organ damage

137
Q

How must someone get sickle cell anemia?

A

Inherit defective gene from BOTH parents to have disease

138
Q

Role of Hgb S in Sickle cell anemia?

A

Causes little problem when properly oxygenated → when O2 drops, fluid polymers realign & cause cell to sickle

139
Q

Role of Hgb S in sickle cell depends on:

A

Dehydration
pH
Oxygenation

140
Q

When a cell sickles what happens?

A

Plug the blood vessels, ↑ viscosity
-Occludes the vessels
-Causes pain
-Infarction

141
Q

Sickled cells pool in …

A

The spleen & hemolyze → & can infarct vessels in the spleen

142
Q

How can sickled cells be reversed?

A

Other chains are normal & will produce Hgb A
-Can return to normal after rehydration & oxygenation

143
Q

When do sickled cells become irreversible?

A

If the plasma membrane is damaged
-The higher # of cells with Hgb S, the higher risk for irreversible sickling → up to 30%

144
Q

Will someone with sickle trait have symptoms?

145
Q

Why are infants with sickle cell okay at first?

A

Their primary Hgb is Hgb F and it takes a few months for the Hgb S to take over

146
Q

Clinical Manifestations of sickle cell anemia

A

Vaso-occlusive crisis
Sequestrian Crisis
Aplastic crisis
Results in severe pain
Can last days to weeks
Can lead to infarcts (CVA/ MI)

147
Q

Clinical manifestations sickle cell

Vaso-occlusive crisis

A

Sickling in microcirculation
Obstructs blood flow
-Creates log jam & no blood can move through vessel

148
Q

Clinical Manifestations sickle cell

Sequestrian crisis

A

Usually only in small children
Large amounts of blood pool in liver & spleen
Causes CV collapse as 20% of blood can pool in liver/spleen

149
Q

Clinical manifestations sickle cell

Aplastic crisis

A

Extreme anemia → ↓ RBCs
Sickled RBC only lives for 10-20 days
Compensatory mechanism in place

150
Q

Dx of Sickle Cell Anemia

A

Mandatory screening at birth
-uses electrophoresis to identify Hgb F from Hgb A & S
Also mandatory screening in college athletes

151
Q

What is the goal of treating Sickle Cell Anemia?

A

To prevent complications & crisis

152
Q

Tx of Sickle Cell Anemia

A

Hydroxyurea → produces more HbF & displaces Hbs
↓ the inflammatory response
Anticoagulation
Pain management

NUR516 (12 decks)

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