Anemia Flashcards
1
Q
Anemia is major ______ condition affecting _____
A
Pathophysiological; RBCs
2
Q
Anemia defined as
A
Reduction in the total # of circulating erythrocytes or a decrease in quality or quantity of Hgb
3
Q
What does a CBC measure?
A
All RBCs & RBC characteristics
Diff types of anemia produce diff CBC results
4
Q
Classification of anemias:
Morphology
A
Size → normo, micro, or macrocytic
Color → normo, hypo, or hyper
other:
- Anisocytic
- Poikilocytosis
5
Q
Anisocytic is defined as
A
Varying sizes
6
Q
Poikilocytosis is defined as
A
Varying shapes
7
Q
Classification of anemias
Measures of morphology
A
Mean corpuscular volume (MCV)
Mean corpuscular Hgb (MCH)
Mean corpuscular Hgb concentration (MCHC)
8
Q
Normal Hematocrit levels
A
Normal: 45%
-Males → 45 - 52%
-Females → 37 - 48%
9
Q
Hematocrit levels in someone with anemia?
A
15%
10
Q
Hematocrit levels in someone with polycythemia?
A
~ 65%
11
Q
What does Reticulocyte count indicate?
A
Bone marrow activity
12
Q
What indicates size of RBCs?
A
Mean corpuscular volume (MCV)
13
Q
What indicates color of RBCs?
A
Mean corpuscular Hgb (MCH)
Mean corpuscular Hgb concentration (MCHC)
14
Q
Solely looking at Hgb & Hct levels cannot ….
A
Make the Dx of anemia!!
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
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
17
Q
Increased reticulocyte is associated with anemia suggesting
A
accelerated destruction or loss of RBCs
18
Q
What % of total RBCs is a normal reticulocyte count
A
~ 1%
19
Q
Polycythemia vera
A
Opposite of anemia
Elevated Hct & Hgb levels
Overabundance of RBCs in polycythemia
20
Q
Primary polycyhtemia
A
Unknown cause
Hyperproliferation of ALL blood cells
-Blood becomes viscous which can ↑ risk of thromboembolisms
21
Q
Secondary polycythemia
A
Known cause
More common & a hyperproliferation of RBCs in response to chronic blood hypoxia (i.e COPD)
22
Q
~ 98% of all polycythemia cases are related to …
A
a mutation in the JAK2 gene
23
Q
Lab studies to Dx anemia
A
CBC
Peripheral blood smear
Iron
Folic acid
BM aspiration &/or biopsy
24
Q
Diagnostic studies to Dx anemia
A
Echocardiogram
Electrocardiogram (ECG)
25
Additional diagnostic tests based on type of anemia
Fecal occult blood test
Vitamin B12 level
26
List 3 causes of anemia
1. ↓ erythrocyte production
2. ↑ erythrocyte destruction
3. blood loss
27
Classic S/S of anemia
**Pallor**
**Fatigue**
**Dyspnea on exertion**
Dizziness
28
Compensatory mechanisms of anemia
Tachycardia
Palpitation
Vasoconstriction
29
Respiratory clinical manifestations of anemia
Tachypnea
Increased depth on respirations
30
Other clinical manifestation Sx of anemia
1. ↑ interstitial fluid into vascular space
2. cold hands & feet
3. chest pain
31
How much blood could an adult lose w/o severe or lasting effects?
500 mL
32
Blood losses of 1000mL or more can have serious adverse effects such as:
Hypovolemic shock
Cerebral hypoperfusion
33
Acute blood loss (anemia)
Rapid loss of blood (hemorrhage) caused by trauma, childbirth, rupture of major BV or organ
34
Severe GI bleeding can occur in what disorders?
Esophageal varices
Penetrating peptic ulcer
35
Pathophysiology of acute blood loss
Hypoxia develops → kidneys produce eryhtropoietin → BM starts to synthesize RBCs → Hypovolemia →RAAS activated (releases ADH)
36
Pathophys of acute blood loss:
When experiencing hypovolemia
Baroreceptors sense a decrease in BP which signals the SNS (increases activity) for the arteries to vasoconstrict in an attempt to ↑ BP
37
Subjective S/S for pt with:
Reduced O2 carrying capacity leading to hypoxia of tissues:
Fatigue
Bone pain from erythropoiesis
Angina
Dyspnea
**↑ RR to ↑ O2 to tissues**
Weakness
38
Objective S/S of pt with:
Reduced O2 carrying capacity leading to hypoxia of tissues:
Tachycardia/ palpitations
Flow heart murmur
Pallor of skin & mucus membranes
> 40% total volume results in profound shock
39
Blood loss from GI tract:
Pts bleeding b/c of esophageal varices often exhibit _____
Hematemesis
40
Blood loss form GI tract:
____ _____ ____ is blood mixed with stomach acid & mucus in vomitus
Coffee ground emesis
41
Blood loss from GI tract:
_____ is blood mixed in stool, causing dark, tarry stool
Melena
42
Blood loss from GI tract:
______ → bright red blood in the stool
Hematochezia
43
Most common causes of Anemia from chronic (slow) blood loss
Peptic ulcer
Inflammatory bowel disease
Colon cancer
Menorrhagia
44
What is menorrhagia?
excessive monthly menstrual loss
45
What is the most common type of Anemia?
Iron deficiency anemia
46
Iron deficiency anemia RBC characterisitcs
Microcytic-hypochromic
47
Iron deficiency anemia is more common in ____
females
48
List the causes of Iron deficiency anemia
Poor dietary intake
Menses
Pregnancy
Ulcerative colitis
Certain medication
Parasitic infections
Neoplasms
Possibly from lead poisoning
49
Iron is the main nutritional element needed for ____ ____
Hgb synthesis
50
How many grams of iron are in the body at any given time?
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)
51
Why is there very little free iron in the body?
Toxic to the cells
52
Iron studies:
Serum iron
Level of circulating iron in the blood
% saturated
-TIBC → % of cells filled w/ transferrin
-Normal → 25-45%
-Iron deficient anemia → < 20%
53
Iron studies:
Ferritin
Protein for iron stores
**Like a bank or pantry**
54
What happens in iron deficient anemia
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
55
Stage 1 iron deficiency anemia
Iron stores for RBC & Hgb synthesis are depleted
-Normocytic/ Normochromic
-Ferritin levels will start to drop
56
Stage 2 iron deficiency anemia
Insufficient levels of iron are taken to the marrow
-Iron deficient RBC production begins
-Cells will begin to ↓ in size & become pale
57
Stage 3 iron deficiency anemia
Hgb deficient cells enter the circulation & replace the dying RBC
-Hgb begins to drop
-Microcytic/ Hypochromic
58
Clinical manifestations of iron deficiency anemia
**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**
59
Epithelial tissue damage in IDA can lead to
Koilonychia → sunken nails
Pallor of conjuctiva
60
Dx of iron deficient anemia
Check Hgb
Check MCV, MCH, MCHC
Serum iron profile
-Iron; TIBC; Tranferrin; Ferritin
BM biopsy/ aspirate
61
Dx of iron deficient anemia
Initially (esp. in chronic slow bleed) what may be the only thing affected?
Ferritin & as it continues the indices, Hgb will be affected
62
Dx of iron deficient anemia
MCV levels
< 80
63
Dx of iron deficient anemia
MCH/ MCHC levels
Low
64
Tx of iron deficiency anemia
Oral iron
-Iron salts
-Orange juice
-Carbonyl iron
-IV iron → dextran
65
Give examples of iron salts
Ferrous sulfate; ferrous gluconate
66
Why is orange juice used to Tx IDA
improves absorption
67
What kind of iron is carbonyl iron?
Pure elemental iron
68
What is the most common oral form of iron?
Ferrous sulfate → contains 65 mg of elemental iron
69
Side effects of ferrous sulfate
GI (Nausea; Heartburn; Constipation)
-Take with food
-makes stool black/ dark green
Teeth staining
-Dilute in juice, drink w/ straw, rinse mouth after
70
Precautions with using ferrous sulfate
Avoid w/ coffee, tea, soda & calcium containing foods
Admin with antacids/ tetracyclines ↓ absorption
71
What type of ferrous sulfate may be easier on the stomach but less effective?
Slow release → less effective as the acid in duodenum protects the iron but the HCO3 from the pancreas can destroy
72
_____ & _____ blockers will ↓ absorption of ferrous sulfate
PPI & H2
73
IV iron
Low molecular weight iron dextran or ferric gluconate
74
Ferric gluconate
Diluted in NSS & infused over 20-60 min
-Test dose (over 5 min) ensure no reaction
75
What can ferric gluconate cause & what is done with infusion?
Can cause prodromal Sx & if bad infusion is stopped & then resumed
76
When is ferric gluconate often used?
Abnormal uterine bleeding
Post partum
Inflammatory bowel disease
CKD
77
Adverse effects of IV irons
Hypotension
Anaphylaxis (Dextran)
-less incidence w/ other IV iron forms
78
Megaloblastic anemia occurs from
Impaired DNA synthesis that causes ineffective erythropoiesis
79
Megaloblastic anemia results in
Large stem cells that mature into large but fragile erythrocytes
-defective cells dying too early which ↓ #s in circulation (eryptosis)
80
CBC characteristics of megaloblastic anemia
Anemia
**Macrocytic**
Normo- or hyperchromic
81
Megaloblastic anemia related to what two deficiencies
Vitamin B12
Folic acid
82
What type of progression is megaloblastic anemia?
Slow progression so Sx only present when advanced
83
Pernicious anemia
AKA: deficiency in vitamin B12
Fatal is left untreated
thought to be autoimmune disorder
84
Causes of pernicious anemia
Conditions that cause malabsorption of B12
↓ intake of B12 products (vegans)
defective gastric secretions of intrinsic factor from parietal cells of gastric mucosa
85
Vitamin B12 is needed for _____ synthesis & _____ maturity
DNA synthesis & nuclear maturity
86
Vitamin B12 prevents
abnormal fatty acids from affecting neural lipids which can result in myelin breakdown
87
Where does vitamin B12 come from?
animal source & binds to intrinsic factor → made from parietal cells in stomach
88
What is necessary for vitamin B12 to be absorbed?
Intrinsic factor
89
Where does intrinsic factor take the vitamin B12?
Takes to ileum where it is released from intrinsic factor & crosses over to blood stream
90
What does vitamin B12 bind to in the bloodstream?
Binds to transcobalamin II which takes it to the storage sites
91
Pernicious anemia has a ____ development so Sx appear in _____ disease
Slow development; Advanced disease
92
Pernicious anemia usually has vague signs such as
fatigue
mood swings
93
Sx of pernicious anemia
Anorexia
weight loss
hyperbilirubinemia
Neurologic (severe)
Hepatosplenomegaly (severe)
94
When could neuro Sx occur in pernicious anemia?
when Hgb < 7 g/dL
95
List neuro Sx of pernicious anemia
Paresthesia of hands & fingers
Ataxia
Memory loss
Vision changes
Weakness, clumsiness, & an unsteady gait
Loss of proprioception
96
Pernicious Anemia is NOT just about IF also from anything that ↓ or eliminates B12 including:
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
Diagnosis of Pernicious anemia
CBC with differential
Vitamin B12 levels
Intrinsic factor
Ab to parietal cells & IF will be found
Bone marrow aspiration
98
Diagnosis of Pernicious anemia
What will you see on CBC w/ differential
Possible low H & H
MCV > 100
MCHC / MHC → normal
99
Tx of pernicious anemia
Vitamin B12 → cobalamin or cyanocobalamin
Oral (if deficiency isn't problem)
-Preferred route
Injection (if deficiency is problem)
-Can be SQ, IM, intranasal
100
How will we know if Tx is working in pt with pernicious anemia?
By rising reticulocyte count & should normalize in 6 wks
101
What do we need folic acid for?
DNA synthesis & red cell maturation (thymine & adenine)
102
Folic acid deficiency anemia
Type of megaloblastic anemia (macrocytic & normochromic)
103
Is folic acid deficiency anemia more or less common than vitamin B12 deficiency?
More common
104
Folic acid deficiency leads to _____ _____ RBCs
Large ineffective RBCs
105
Where can folic acid be found?
Vegetables
Fruits
Cereals
Meat (but lost in cooking)
106
How much folic acid does the body store?
500-20,000 mcg & needs 50-100 mcg/day
107
When will anemia occur from folic acid dietary deficiency?
Within a few months
108
Who is at risk for folic acid deficiency?
Pregnancy & lactation
Alcoholics
Fad diets
Individuals w/ celiac or inflammatory bowel disease
Chronic inflammatory disorders
109
Why are pregnant & lactating clients at ↑ risk for folic acid deficiency?
Their needs increase 5-10x
-Needed for neural tube development so supplement very important
110
Why are alcoholics at ↑ risk for folic acid deficiency?
Interferes with folate metabolism
111
Why are people who follow fad diets at ↑ risk for folic acid deficiency?
Decreased folate intake
112
What types of chronic inflammatory disorders have ↑ risk for folic acid deficiency?
rheumatoid arthritis
tuberculosis
psoriasis
bacterial endocarditis
systemic infections
113
Clinical manifestations of Folic acid deficiency
Classic signs of anemia
No neuro Sx
Manifestations r/t malnourishment
undiagnosed IBD
114
List some manifestations r/t to malnourishment in folic acid deficiency
Cheilosis
Stomatitis
Burning mouth syndrome
Dysphagia
Flatulence
GI disturbances
115
Diagnosis of Folic acid deficiency:
CBC
**Will see changes in indices before Hgb**
MCV > 100
MCHC & MHC → normal
116
Diagnosis of Folic acid deficiency:
What levels will be low?
Folic acid levels
117
Tx of folic acid deficiency:
Folic acid requires ____ to be converted to ____ ____
B12; active form
118
Tx of folic acid deficiency:
Two forms:
Active & Inactive
119
Which form of folic acid is more common for Tx of folic acid deficiency?
Inactive
120
Inactive form of folic acid
Folate
Can be given PO, IV, SQ, IM
Tx with supplementation
121
What labs are important to monitor for a pt w/ folic acid deficiency?
Hgb & reticulocyte count
122
Aplastic Anemia Results from ...
Breakdown in production in BM stem cells that inhibit growth of RBC, WBC, & PLTs
123
Aplastic anemia results as failure of the _____ to replace the ____ red cells as they are destroyed & leave the _____
Marrow; senescent; circulation
124
Characteristics of RBCs in Aplastic anemia
Cells are normal size & color
125
What happens in Aplastic anemia due to WBCs & PLTs having shorter life spans?
The disease often presents with infection or bleeding
126
Describe onset of aplastic anemia
Can be either abrupt or gradual
127
Causes of Aplastic Anemia
Radiation exposure
Chemo → inhibits hematopoiesis
Chemicals → Benzene
Viral illness (Hepatitis, mono, HIV)
Pregnancy
Unknown → ~ 2/3 cases
Cytokines suppress normal stem cell development
128
Diagnosis of Aplastic Anemia
CBC → shows pancytopenia
-WBCs → < 200/mm3 (↑ risk of opportunistic infections)
-RBCs → normocytic/ normochromic
129
Symptoms of Aplastic Anemia
Infection
Fatigue, pallor, weakness
Petechiae/ Purpura
Ecchymosis
Bleeding from body orifices
130
Tx of Aplastic Anemia
**Treat underlying cause**
**BM transplant from sibling donor → preferred Tx**
Prophylactic Abx & PLT, RBC, & WBC transfusions may be required
BM Stimulants
131
Tx of Aplastic Anemia:
List two bone marrow stimulants
Filgrastim (NeupogenR)
Epoetin-alfa (EpogenR)
132
Hemolytic anemia can be ____ or ____
Acquired or Hereditary
133
Acquired hemolytic anemia results from
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
Hereditary hemolytic anemia results from
Structure deficits
Enzyme deficiencies
Defects in globin synthesis or structure
-Sickle cell
-Thalassemia
135
Sickle cell anemia has highest concentration in
African Americans, Middle East, & Mediterranean countries
136
What is sickle cell anemia?
Inherited defect of Hgb S → leads to hemolytic anemia & chronic organ damage
137
How must someone get sickle cell anemia?
Inherit defective gene from BOTH parents to have disease
138
Role of Hgb S in Sickle cell anemia?
Causes little problem when properly oxygenated → when O2 drops, fluid polymers realign & cause cell to sickle
139
Role of Hgb S in sickle cell depends on:
Dehydration
pH
Oxygenation
140
When a cell sickles what happens?
Plug the blood vessels, ↑ viscosity
-Occludes the vessels
-Causes pain
-Infarction
141
Sickled cells pool in ...
The spleen & hemolyze → & can infarct vessels in the spleen
142
How can sickled cells be reversed?
Other chains are normal & will produce Hgb A
-Can return to normal after rehydration & oxygenation
143
When do sickled cells become irreversible?
If the plasma membrane is damaged
-The higher # of cells with Hgb S, the higher risk for irreversible sickling → up to 30%
144
Will someone with sickle trait have symptoms?
NO
145
Why are infants with sickle cell okay at first?
Their primary Hgb is Hgb F and it takes a few months for the Hgb S to take over
146
Clinical Manifestations of sickle cell anemia
**Vaso-occlusive crisis**
**Sequestrian Crisis**
**Aplastic crisis**
Results in severe pain
Can last days to weeks
Can lead to infarcts (CVA/ MI)
147
Clinical manifestations sickle cell
Vaso-occlusive crisis
Sickling in microcirculation
Obstructs blood flow
-Creates log jam & no blood can move through vessel
148
Clinical Manifestations sickle cell
Sequestrian crisis
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
Clinical manifestations sickle cell
Aplastic crisis
Extreme anemia → ↓ RBCs
Sickled RBC only lives for 10-20 days
Compensatory mechanism in place
150
Dx of Sickle Cell Anemia
**Mandatory screening at birth**
-uses electrophoresis to identify Hgb F from Hgb A & S
**Also mandatory screening in college athletes**
151
What is the goal of treating Sickle Cell Anemia?
To prevent complications & crisis
152
Tx of Sickle Cell Anemia
Hydroxyurea → produces more HbF & displaces Hbs
↓ the inflammatory response
Anticoagulation
Pain management
