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21 Cards in this Set

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What do low levels of Hb result in?
weakness, pallor, DARK URINE, jaundice, ABDOMINAL PAIN, and DARK SPOTS on the RBC
Anemia
Decrease of Hb concentration below normal levels
Men: 14-18
Women: 12-16
Is a SYMPTOM not a disease
Hematocrit
Simple but crude test for anemia
% of the volume of a blood sample occupied by cells
<42% Men
<37% Women
Sources of Anemia
Decreased production of erythrocytes
Iron Deficiency: Inhibits heme production - 2 types
Microcytic: Small RBC
Hypochromic: Pale RBC
Folate or B12 Deficiency: Nucleotide synthesis inhibited which inhibits DNA synthesis so rather then cell divides becomes larger called Megoblastic (Pernicious) - Large RBC
Sources of Anemia
Increased loss or Destruction of erythrocytes
From Bleeding, Immune hemolysis, PYRUVATE kinase or HEXOKINASE deficiency, Sickle Cell Anmeia, G6PD Deficiency
Last 4 ALL cause Hemolytic Anemia
Hemolytic Anemia
Contents of RBC leak out, which causes the release of Hb
When and how is damaged caused by hemolytic anemia?
Heme is volatile in the body and albumin binds it. When the levels of heme are to high to be bound it can cause damage
Symptoms of Hemolytic Anemia
Weakness upon exertion - ATP under produced; low O2
Pallor: Especially in gum and nail beds
Jaundice: Noticable in sclera of eyes due to bilirubin
Unconjugated bilirubin will not be excreted in urine so results in dark urine
Pathway of Energy Metabolism in Human Erythrocyte
Look in notes
What may help determine the half-life of RBC
Hexokinase
What can you take to increase the store of blood?
Adenosine
Methemoglobin (MetHb)
Adding an electron to O2 creates a superoxide or H2O2 which will oxidize iron to Fe3+ which cannot bind to O2 instead binds H2O
Pt. will look blue
NADH and Cyto. Reductase reduce these compounds
What do some maleria drugs do?
Make Hb into MetHb because of the higher rate of RBC turnover gets rid of the maleria
Methemoglobinemia
Cytochrome B5 Reductase Deficiency
Methemoglobin Reductase is dependent on NADH from Glycolytic
Tyrosine is accompanied
Generation of Superoxide Ions
Most come from ETC
Neutralization of Superoxide
Reduced to H2O2 by Superoxide Dismutase
H2O2 is then converted to water by either CATALASE or GLUTATHIONE PEROXIDASE which requires NADPH from PPP
Hexokinase Deficiency
Glycolytic Pathway and PPP are SLOWED down
Decreased ATP, NADH & NADPH
Unable to maintain ion pumps
Chronic Hemolytic Anemia
Treament: Splenectomy
May determine the lifespan of RBC
Pyruvate Kinase Deficiency
Prominent in the Amish b/c of intermarriage creates Homozygotes
Chronic Hemolytic, Jaundice, Pallor, Gall Stones, Weakness
Parvovirus infection results
What are the main problems with Pyruvate Kinase Deficiency?
Low ATP which affects membrane integrity and High Conc. of 2,3 bisphosphoglycerate
PPP and NADPH also affected but not as much as Glycolytic
G6PD Deficiency
Can be acute or chronic hemolysis
Fave beans aggravate the disease
Possible evolutionary in the body's fight against Maleria
Heinz bodies produced
Similar to Primaquine
Heinz Bodies
Rigid aggregates of oxidized Hb
Oxidation of the disulfide bonds causes them to precipate out of RBC