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N351: Pathophysiology I > Module 3 > Flashcards

Module 3 Flashcards

1
Q

Composition of Blood

A

45%RBC
50% Water
About 5% Formed Elements - Plasma Substances
Less than 1% Buffy Coat of WBC above RBC layer

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2
Q

Composition of Formed Elements

A

99% Erythrocytes
Leukocytes
Thrombocytes

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3
Q

Composition of Blood Plasma

A

-90% Water
-Plasma Proteins (Albumin, Globulins, Fibrinogen)
-Electrolytes, dissolved gasses, waste products of metabolism, nutrients, vitamins, cholesterol

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4
Q

Albumin

A

Plasma protein essential in wound healing, oncotic pressure establishment, and colloid osmotic pressure in capillary dynamics

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5
Q

Globulins

A

Plasma proteins that participate in the specific immune response. They are made by B cells/Plasma Cells

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6
Q

Fibrinogen

A

Plasma protein that is a component of the clotting cascade (through stabilizing the clots)

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7
Q

Examples of Waste Products in the Blood from Metabolism?

A

Urea
Creatinine

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8
Q

Pancytopenia

A

Anemia where a person has a low count for all 3 types of formed elements (Thrombo-, Leuko-, Erythro-)

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9
Q

Most abundant plasma protein?

A

Albumin

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10
Q

Kupffer Cells

A

Macrophages of the liver

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11
Q

Hematopoiesis

A

Production of blood elements through the differentiation of stem cells

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12
Q

Pluripotent “Hematopoietic” Stem cells

A

“Mother Cells” that are the source of ALL blood cells and are located in bone marrow

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13
Q

Progenitor Cell

A

A differentiated pluripotent stem cell that is now committed to one particular lineage of blood cell

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14
Q

Growth Factors

A

Factors stimulating the growth and differentiation of progenitor cells into one of the forms of formed elements

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15
Q

Erythrocyte Growth Factor

A

Kidney Erythropoietin

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16
Q

When does the kidney release erythropoietin?

A

When it detects low oxygen levels in blood (hypoxia, smoking, etc)

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17
Q

5 Types of Progenitor Cells?

A

Pluripotent Stem Cell –> Erythroblast, Myeloblast, Monoblast, Megalokaryoblast, Prolymphoblast

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18
Q

Erythroblast Differentiation Line

A

Erythroblast –> Reticulocyte –> Erythrocyte

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19
Q

Myeloblast Differentiation Line

A

Myeloblast –> Granulocyte –> Eosinophil, Basophil (mast cell), Neutrophil

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20
Q

Monoblast Differentiation Line

A

Monoblast –> Monocyte –> (in tissue) Macrophage

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21
Q

Megalokaryoblast Differentiation Line

A

Megalokaryoblast –> Break apart into Platelets

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22
Q

Prolymphoblast Differentiation line

A

Prolymphoblast –> Lymphoid Stem Cell –> B and T Lymphocytes –> Plasma Cell and Killer T Cell respectively

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23
Q

What is the main take away for cellular differentiation?

A

The mother cell becomes a progenitor cell that chooses a line to follow and STICKS WITH IT

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24
Q

Difference between Differentiation and Proliferation?

A

Differentiation is cell maturation and Proliferation is just an increase in cell numbers

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25
Q

Are growth factors specific or non specific?

A

Both, some act on several progenitor cells and some are for specific lines

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26
Q

Growth factors for specific lines of cells are called…

A

Colony Stimulating Factors

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27
Q

GCSF

A
  • Granulocyte Colony Stimulating Factor
  • GF for granulocytes
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28
Q

Erythropoietin

A

-GF for erythrocytes coming from the kidneys

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29
Q

Many growth factors are…

A

Cytokines (from the immune and inflammatory cells)

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30
Q

As a growth factor, Cytokines can control…

A

blood cell amount

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31
Q

RBC have no what?

A

Nucleus, Mitochondria, Ribosomes, Reproduction Ability

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32
Q

What does the shape of the RBC allow for?

A

The bi concave disk shape allows for a high SA to allow rapid diffusion, and with it being small and flexible allows for it to rapidly diffuse into capillary beds

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33
Q

Erythropoiesis

A

process of growth for RBC using the growth factor erythropoietin

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34
Q

Lifespan of RBC

A

120 days

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35
Q

Timeline of an RBC

A

Unipotential Stem Cell meets Erythropoietin to produce an Erythroblast in about 6 days, The reticulocyte then stays for 1 day in the marrow and then remains for a day in the blood as a nucleated reticulocyte before becoming an erythrocyte for 120 days in the blood

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36
Q

Building blocks of Erythropoiesis?

A

Iron, Folic acid, Vitamin B12

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37
Q

Reticulocytes in the bloodstream are important because?

A

They show the bone marrow is working

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38
Q

How are reticulocytes different from erythrocytes?

A

they are bigger and have part of the retained nucleus

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39
Q

What occurs when RBCs reach the end of their 120 day cycle?

A

The RBC disintegrates, releases Hgb and components into the blood circulation

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40
Q

What phagocytizes old RBC?

A

the liver and the spleen

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41
Q

What occurs to RBC globulin after phagocytosis?

A

its converted to Amino acids

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42
Q

What occurs to RBC iron after phagocytosis?

A

its stored int the liver and spleen until transferring carries it to the bone marrow to make more Hgb

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43
Q

What occurs to the majority of the RBC molecule after phagocytosis?

A

It is converted to bilirubin and excreted as bile/in urine

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44
Q

How do rates of destruction and synthesis relate in good health?

A

Rate of Destruction = Rate of Synthesis

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45
Q

Composition of Hemoglobin?

A

Heme (iron) and Globulin proteins

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46
Q

How many binding sites does an RBC have?

A

1200 (300 Hgb per molecule * 4 binding sites per Hgb)

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47
Q

Why are the 100 abnormal types of Hgb abnormal?

A

they carry O2 poorly, do not carry O2 at all, or do not survive a full 120 days

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48
Q

Hematocrit (Hct)

A

Percentage of blood that is red blood cells

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49
Q

What is the normal Hct value?

A

45%

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50
Q

Why is Hct not as useful?

A

its a percentage (relative) so an abnormality could occur with a normal Hct level

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51
Q

Mean Corpuscular Volume

A

Relates to Cell Size
> MCV = Hct/RBC

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52
Q

Microcytic

A

cells too small in size (low MCV)

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53
Q

Normocytic

A

cells normal in size

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54
Q

Macrocytic

A

cells too large in size (high MCV)

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55
Q

Mean Corpuscular Hemoglobin Concentration

A
  • Weight of Hgb per volume RBCs
    -MCHC = Hgb/Hct
    -When we discuss this we are talking about the cell color (due to iron)
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56
Q

Hypochromic

A

cells with too little Hgb (less red)

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57
Q

Normochromic

A

cells with a normal amount of Hgb

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58
Q

Hyperchromic

A

Cells with too dense Hgb (very red)

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59
Q

Mean Corpuscular Hemoglobin

A
  • Less important
    -Average Hgb weight in each RBC (MCH = Hgb/RBC)
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60
Q

Why is Mean Corpuscular Hemoglobin less important?

A

it Reflects BOTH size of RBC and concentration of Hgb in the RBC (Color) so it is hard to interpret

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61
Q

What does a low MCH value mean?

A

Hypochromia OR Microcytosis OR both

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62
Q

Red Cell Distribution Width (RDW)

A
  • standard deviation of MCV (Size)
    -its a measure of the degree of uniformity of the RBC sizes (uniformity amongst all of them)
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63
Q

Exception to RDW measures?

A

Thalassemia

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64
Q

Thalassemia

A
  • Genetic anemia for people of Mediterranean or SE Asian descent
  • the RBC are a uniform cell size, but there is less Hgb leading to anemia
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65
Q

Key point to remember about RDW uniformity?

A

The cells are the same size, but the size might be abnormal

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66
Q

Low degree of RBC uniformity leads to…

A

A higher RDW value

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67
Q

RDW has____ sensitivity and ___ specificity

A

high sensitivity and low specificity

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68
Q

What does a normal RDW value say?

A
  • You can rule out iron deficiency anemia since it has a high RDW (high sensitivity), but you cannot rule out anemia (low specificity)
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69
Q

RDW tells us about RBC size problems, but not if the mean is too low, high, or normal - to know that you must look at …

A

MCV (Mean Corpuscular Volume)

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70
Q

Reticulocyte Count

A

-A very important measure
- Indicates the number of RBCs containing RNA (ones that have not disposed of the nucleus entirely yet)

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71
Q

When you have a reticulocyte count you need to know …

A

if kidney function is great, because if it is bad then there is no erythropoietin

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72
Q

Increased Erythropoietin leads to

A

Increased reticulocyte amount

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73
Q

Reticulocyte Count is a good indicator of …

A

bone marrow function

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74
Q

Reticulocyte count is the …

A

-most reliable measure of RBC production (when looking at absolute rather than relative)
- Absolute = %Reticulocytes * RBC count

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75
Q

Spherocytes

A

Abnormal small and round morphology of RBC

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76
Q

Elliptocytes

A

-Abnormal Elliptical or Oval morphology of RBC
-causes more hemolysis

77
Q

Sickle

A

Abnormal crescent morphology of RBC that clogs and can cause sickle cell crisis

78
Q

Target Cell Morphology

A
  • RBC cells that are thin with less Hgb causing it to look like a bullseye
79
Q

Anisocytosis

A

Peripheral smear abnormality where the RBC has an abnormal SIZE due to severe anemia

80
Q

Poikilocytosis

A

Peripheral smear abnormality where the RBC has an abnormal SHAPE due to severe anemia

81
Q

Spherocytosis

A

Peripheral smear abnormality where RBCs have spherical cells without pallor center (pale) due to hereditary pherocytosis

82
Q

Stromatocytosis

A

Peripheral smear abnormality where RBCs have slit like areas of central pallor rather than round due to congenital hemolytic anemia

83
Q

Target Cell Abnormality

A

Peripheral smear abnormality where RBCs have dark centers and periphery with a clear ring in between them due to Thalassemia and hemoglobinopathies

84
Q

Basophilic Stippling

A

Peripheral Smear Abnormalities where RBC have punctuate stippling when wright stained DUE TO LEAD POISONING!

85
Q

What are the causes of anemia?

A

Decreased RBC, Decreased Hgb, or Decreased Hct due to:
1. Disorder in RBC production
2. Elevated Loss of RBC
3. Absence of some substrate like globulin proteins, heme, folic acid, B12, etc

86
Q

What determines the symptom expression of anemia

A
  1. Duration and Severity
  2. Age and Health Status
87
Q

Hypoxemia

A

manifestation of anemia due to lack of oxygen dissolved in the blood

88
Q

Manifestations of Hypoxemia

A

Pallor
Weakness
Listlessness
Fatigue
Increased Respiratory Rate to try and compensate
Increased heart Rate (Which can lead to more issues when there is prexisting cardiovascular issues like heart failure, angina, and intermittent claudication
dizziness
palpatations
giddiness

89
Q

Intermittent Claudication

A

No enough blood flow and oxygen to the legs due to arteries (feels better to stop doing things that increase metabolic demand and just stand in place to help blood move down)

90
Q

What things determine anemia classification?

A
  1. Rate of Development
  2. Morphology (Shape)
  3. Hemoglobin Content
  4. Type of Defect or Etiology
91
Q

Acute Anemia

A

severe, rapid blood loss (hemorrhage)

92
Q

Chronic Anemia

A

gradual blood loss or other chronic condition that results in anemia

93
Q

Production Defect

A

the bone marrow can function , so some building block necessary is missing/low

94
Q

Destruction Defect

A

Two fold: Either bone marrow is getting destroyed or hemolysis is occurring

95
Q

Normal reticulocyte counts indicate what?

A

a Destruction defect since production is working - a low count would indicate a production defect where we lack building blocks

96
Q

Microcytic Hypochromic Anemias

A

Iron Deficiency
Thalassemia
Chronic Systemic Diseases

97
Q

Microcytic Normochomic Anemia

A

Chronic systemic disease

98
Q

Normocytic Normochromic Anemias

A

Anemia of chronic disease
Acute blood loss
Hemolytic anemia
renal failure
liver disease
hypothyroidism
sickle cell anemia
hypersplenism
aplastic anemia

99
Q

Normocytic Hypochromic Anemias

A

Lead poisoning (plumbism)
chronic systemic disease

100
Q

Normocytic Hyperchromic Anemia

A

Hereditary Spherocytosis

101
Q

Macrocytic Normochromic Anemias

A

Folic Acid deficiency
Alcoholism
B12 deficiency
hypothyroidism
chronic liver disease
drug induced (chemotherapy)

102
Q

Macrocytic Hypochromic Anemia

A

some macrocytic anemias with superimposed iron deficiency

103
Q

Anemias caused by a disorder of red blood cell production is due to?

A
  • Inadequate or inaccessible iron
    -lack of folic acid OR VB12 OR globulin
    -bone marrow disease like leukemia
    -erythropoietin deficiency from renal failure
104
Q

Most common anemia globally?

A

Iron Deficiency Anemia (Microcytic, Hypochromic)

105
Q

Aplastic Anemia

A

-Anemia caused by bone marrow failure
-Production issue
-Can be due to idiopathy, radiation, chemotherapy - but generally we do not understand why

106
Q

What do lab indicators show about Aplastic Anemias?

A

-Normocytic Cells
-Normochromic cells
-Decreased Reticulocyte count

107
Q

Signs and Symptoms of Aplastic Anemia?

A

-Hypoxemia
-Decrease in bone marrow function (myelosuppression)
-Infection
-Bleeding

108
Q

Aplastic Anemia Treatments?

A

-Stopping drugs and chemo therapies
- blood transfusions
-possible bone marrow transplant

109
Q

Causes of Iron Deficiency Anemia?

A
  • Decreased iron Intake
    -Decreased Iron absorption
    -chronic blood loss
110
Q

Lab results indicating Iron deficiency Anemia?

A
  • Microcytic (low MCV)
    -Hypochromic (Low MCHC)
    (low iron availability and lower Hgb production as well)
111
Q

Most common anemia?

A

Iron deficiency anemia

112
Q

Most common cause for iron deficiency anemia?

A

Chronic Blood los (i.e. excessive menstrual cycle loss, 75 mL blood occult loss per day due to GI bleed)

113
Q

Serum Iron Test

A

-not very useful (influenced by many things)
this test looks at iron bound to transferrin (serum iron) - so it tells us rate of delivery to tissues, but not amount stored in tissues.
-Hemolysis, time of day, menstruation, transfusion, etc all can alter the value

114
Q

Where is iron throughout the bdoy?

A

70% is in the Hgb of RBC, 30% is stored in tissues as ferritin and hemosiderin

115
Q

Serum Ferritin Test

A

-Meaningful iron test
-Measures iron stores in body (ferritin is 23% of iron stored in the liver/marrow/spleen)
-The amount of ferritin directly relates to total body stores (like savings in a bank)
- blood transfusions will not affect values, but chronic inflammation will

116
Q

Best marker for iron deficiency anemia?

A

Serum ferritin

117
Q

What can falsely impact serum ferritin levels?

A

tissue damage leading to chronic inflammation, malignancy, or hepatitis, and Acute or Chronic illness

118
Q

How fast can serum ferritin levels be fixed with supplements?

A

In 2-3 weeks for oral administration, 24 hours for parenteral

119
Q

Transferrin

A

-Globulin in the blood that binds and transports iron to the bone marrow to make Hgb
-1/3 of it is bound with iron
-1 week half life

120
Q

Transferrin Concentration Test

A

-measures concentration of transferrin in the blood which is inversely proportional to the amount of iron stored in the body
-the value comes either directly or from estimating the total iron binding capacity (TIBC)

121
Q

TIBC

A

-Maximum iron binding capacity of Transferring and other iron binding globulins
-This is not always done because it indicates liver function moreso than iron stores

122
Q

As stores of iron increase…

A

transferring levels decrease

123
Q

Things that influence transferrin concentrations?

A

inflammation, loss of proteins, nutritional status, liver disease

124
Q

Transferrin Saturation Test

A

-The percentage of transferrin and other mobile iron binding proteins that are saturated by iron
-Transferrin Saturation (%) = (Serum iron Level/TIBC) x 100%
-20-50% is normal (half bound then go to marrow)

125
Q

Transferrin Saturation as A Bus Analogy

A

-TIBC/Max Iron Binding capacity = # empty seats
-Transferrin Saturation = # of occupied seats
- bus = transferrin
-iron = kids
-More busses on the way = low serum ferritin

126
Q

Things leading to high Transferrin Saturation?

A
  • Iron Overload
  • Hemochromatosis (over absorption) - leads to liver and spleen being full so other areas get iron and are injured as a result
127
Q

We can treat iron deficiency with …

A

Dietary iron

128
Q

Amount of dietary iron and how it is absorbed?

A

-10-20 mg in the diet, but only 10% is absorbed in the duodenum and upper jejunum

129
Q

Dietary Iron storage amount?

A

5001-500 mg as ferritin and hemosiderin in liver/spleen/marrow/skeletal muscles/etc

130
Q

Reasons you might be losing a lot of your dietary iron?

A

Menstruation or Pregnancy/Childbirth

131
Q

Manifestations (S/S) of Iron Deficiency Anemia

A

-Same anemia symptoms
-brittle spoon shaped nails
-glossitis
-pica
-web in upper esophagus (rare)
-hypoxemia

132
Q

Glossitis

A

red, smooth, sore tongue

133
Q

Pica

A

habitual eating of non-nutritive substances

134
Q

How to treat iron deficiency anemia?

A
  • CORRECT THE ROOT CAUSE! (e.g. bleeding)
  • give ferrous sulfate dietary supplements either orally or parenteral in deep muscle
    -Reticulocytosis will occur in 4-5 days, but therapy must
    continue for at least 6 months to restore stores
    -Transfusions when case is severe
135
Q

Precautions when giving Ferrous Sulfate?

A

Must be given with food since it irritates the gastric mucosa, and it must be given in a liquid form through a straw since it will permanently stain teeth

136
Q

Megaloblastic Anemias

A

-anemia where the RBC are too big (macrocytic) with an increased MCV
-due to impaired synthesis of DNA most likely from folic acid or VB12 deficiency
-Increased MCV, Decreased Lifespan and Amount
-Possible decrease in WBC, PLT, RETICULOCYTES

137
Q

Vitamin B12

A
  • Vitamin in our food supplied from meat, eggs, milk, and cheese
    -Absorbed in the terminal ileum of the S. Intestine when bound to intrinsic factor from the parietal cells
    -Liver is full of VB12
138
Q

Intrinsic Factor

A

a mucoprotein secreted by the gastric mucosa parietal cells necessary for complexing with VB12 in order for absorption to occur

139
Q

What does the large VB12 stores in the liver mean for anemia?

A

VB12 deficiency anemia (megaloblastic) will not occur for years potentially

140
Q

Causes of Vitamin B12 Megaloblastic Anemia?

A
  • Lack of intrinsic factor
    -dietary inadequacy
    -ileum or parietal cell defects decreasing absorption
    -parasites or unusual bacteria
141
Q

Serum Vitamin B12 and Folate Lab Test

A
  • looks at VB12 and Folic acid together
  • use to check for megaloblastic anemia
142
Q

Interfering Factors for VB12 and Folate levels in laboratory tests?

A

-For VB12: increases occur in pregnancy, with use of oral contraception, high V A and C levels, smoking
-For Folate: antagonists, hemolysis, transfusions

143
Q

There is not necessarily what for Folic Acid storage?

A

large stores like in VB12

144
Q

Cobalamine

A

dietary form of vitamin B12

145
Q

Intrinsic Factor Antibodies Laboratory Test

A

-checks intrinsic factor levels for VB12 transport to liver or marrow
-checks for Pernicious anemia

146
Q

Pernicious Anemia

A
  • Pernicious means Dangerous
    -autoimmune
    -Anemia due to either:
    Type 1 Antibodies - blocks bonding of cobalamine and I factor, destruction of gastric parietal cells (in gastric area)

OR

Type 2 Antibodies - blocks binding of complex to the ileal receptors, intefering in ileal area

147
Q

Causes of Vitamin B12 Deficiency

A
  • Decreased intake (poor diet)
    -Decreased Intrinsic Factor ( total gastrectomy)
    -Alcohol use (poor absorption and diet/nutrition)
    -Pernicious anemia
    -Spruce and Celiac Disease (maladsorption)
    -Ileum Resection
    -Pregnancy requirements causing increased need
148
Q

What do lab tests show about VB12 deficiency anemia?

A

-Macrocytic
-Normochromic
-Decreased VB12 levels

149
Q

Signs and Symptoms of VB12 Deficiency

A

-typical anemia symptoms
-Hypoxemia
-insidious symptoms
-premature grey hair
-splenomegaly
-yellow blue color blindness
-low BP
-vitiligo
-lemon yellow skin color
-low grade fever
-NEUROLOGIC SYMPTOMS (parasthesias)

150
Q

Parasthesias

A

Numbness and tingling due to neurologic issues

151
Q

Vitamin B12 Deficiency Treatments

A
  • Increase in VB12 in diet
    -Parenteral vitamin B12 (to bypass the gut antibodies from pernicious anemia)
152
Q

Neurologic Symptom progression for VB12 deficiency

A

Early - inability to do fine movements and loss of vibratory sense (2 point discirimination)

Progressive - Parasthesias, weakness, uncoordination, ataxia, personality changes

Late - incontinence, spastic paralysis, confusion, psychosis

153
Q

Why is VB12 Deficiency Insidious?

A

symptoms occur slowly (not at least for a year)

154
Q

Vitiligo

A

condition that causes depigmentation of sections of the skin due to autoimmune reasons

155
Q

Why does VB12 deficiency cause neurologic symptoms?

A

because VB12 is crucial to production and maintenance of the myelin sheathe

156
Q

Ataxia

A

uncoordinated walk

157
Q

Folic Acid Deficiency Anemia

A

-Megaloblastic anemia due to issues with folic acid/folate amounts for Hgb/RBC production

158
Q

Causes of Folic Acid Deficiency

A

-Decreased Folate intrake
-Alcohol Abuse
-Increased need due to pregnancy and lactation
-Folic acid antagonists

159
Q

What do laboratory tests reveal during folic acid deficiency?

A

-Macrocytic
-Normochromic
-Decreased amounts of serum folate in the liver/tissues

160
Q

Signs and Symptoms of Folic Acid Deficiency?

A

-Universal Anemia symptoms
-hypoxemia
- NO NEUROLOGIC SYMPTOMS

161
Q

Treatment of Folic Acid Deficiency?

A

-increased folic acid intake
-dietary supplements
-ceasing antagonist meds like those for rehumatoid arthritis

162
Q

Low folic acid levels in pregnancy lead to…

A

neurotube defects in child

163
Q

Major difference between VB12 and Folate deficiency anemia?

A

VB12 has neurologic symptoms occuring

164
Q

Anemia due to Blood loss

A

-can either by from acute or chronic blood loss

165
Q

Cause of acute anemia due to blood loss

A

trauma, surgery, hemorrhaging

166
Q

cause of chronic anemia due to blood loss

A

GI bleed, ulcer, menstruation

167
Q

Lab results for acute anemia due to blood loss

A

-normocytic
-normochromic
-increased reticulocyte count

168
Q

Lab results for chronic anemia due to blood loss

A

-microcytic
-hypochromic
-increased reticulocyte count

169
Q

Signs and Symptoms of acute anemia due to blood loss

A

-Volume depletion
-decreased BP and increased heart rate leading to shock

170
Q

Signs and Symptoms of chronic anemia due to blood loss

A

hypoxemia

171
Q

Treatment for acute anemia due to blood loss

A

-Hemostasis
-oxygen
-transfusion
>anything to stop bleeding out/shock

172
Q

Treatment for chronic Anemia due to blood loss

A

-treat the underlying cause
-iron therapy oftentimes

173
Q

Chronic anemia due to blood loss is often …

A

iron deficiency anemia

174
Q

Why do you not want to treat chronic anemia due to blood loss with blood transfusions?

A

It can tell bone marrow to stop working which could lead to RBC,WBC,PLT creation shutdown (pancytopenia)

175
Q

Anemia of inflammation and chronic disease

A
  • second most common cause of anemia behind iron deficiency
    -Anemia where the substrates are fine leading to normocytic, normochromic (or slightly hypochromic) RBC - but their survival is shortened and cannot be compensated/treated because inflammation interferes
    -Rate of Destruction > Rate of Production (imbalance)
176
Q

What happens to reticulocyte count in anemia of inflammation and chronic disease?

A

The count is low since this anemia does not respond to any known therapy

177
Q

Polcythemia

A

-Opposite of Anemia
-Abnormally high total red cell mass (all cell lines: so WBC and PLT too)
-2 types - Relative, and Absolute with Primary and Secondary subtypes

178
Q

Relative Polycythemia

A

-fluid loss without cellular loss
-Loss of plasma volume leading to a high Hct (50% rather than the normal 40-45)

179
Q

Causes of Relative Polycythemia

A
  • loss of fluid but not cell loss
    ex: Diarrhea, Profuse Sweating, Dehydration
180
Q

Absolute Polcythemia

A
  • increase in the actual number of RBC
    -2 subtypes: Primary and Secondary
181
Q

Polycythemia Vera

A

-Absolute Primary Polycythemia
- proliferative disorder common in men 40-60 y/o where the blood gets very viscous (and Hct can reach 80%!! - the same as in packed blood transfusions)

182
Q

Secondary Absolute Polycythemia

A

-Chronic hypoxia leading to the kidney increasing erythropoietin levels thus causing more cells
-ex: high altitude, smoking, COPD, tumors, heart and lung diseases can cause the hypoxia

183
Q

Complications due to Polycythemia

A
  • Increased blood viscosity interfering with cardiac flow
    -Hypertension
    -Venous stasis
    -Thromboembolism potential (leading to stroke, heart attack, or deep vein thrombosis)
184
Q

Venous Stasis

A

-opposite of intermittent claudication
-pooling of blood in veins leading to little clots causing the legs being unable to return blood to the heart

185
Q

How to treat venous stasis?

A

elevate legs to return blood to heart

186
Q

How to treat intermittent claudication?

A

lower legs to help arterial problems move blood into the legs

187
Q

Treatment for Relative polycythemia

A

fluids

188
Q

Treatment for polcythemia vera

A

Making the blood less viscous through normal saline, medication, bone marrow transplants, drug therapy, or periodic phlebotomy

189
Q

Treatment for secondary polcythemia

A

Oxygen at appropriate levels to stop hypoxia (be careful when dealing with a COPD patient)

N351: Pathophysiology I (11 decks)

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