Flashcards in Blood Deck (34)
Where do formed elements in blood come from?
Pluripotent stem cell
WBC, RBC, platelets
What can cause cyanosis?
Cyanosis: lips/fingertips/skin turn blue
Cause: lot of Hb that doesn't have O2 bound
Hematocrit=% of blood that is cells
-after menopause, women's levels go to what men's areo
What does hypoxia, low O2 delivery to kidney's signal?
↑ HIF (TF for erythropoietin) → makes erythropoietin → more RBC's
*erythropoiesis (making RBC)=occurs in bone marrow
What does the kidney do?
Senses O2 levels in tissues
If low O2 to KIDNEY→ kidney gets more HIF→ ↑ erythropoietin (EPO)
*HIF is destroyed by O2, so high O2 will destroy HIF and thus body won't make more RBC/erythropoietin (EPO)
"We're in a hurry and need RBC's!!!"
A peptide hormone (travels in blood) secreted by the kidneys that increases the rate of production of red blood cells in response to falling levels of oxygen in the tissues
Receptor: in JAK2/STAT5 pathway→ "growth"
-Acts on stem cells→ ↑ differentiation→proerythroblasts→RBC
-↑ maturation rate (makes mature faster)
-↑ transferrin (transport protein for Fe) & its receptor
Not enough Fe→
microcytic anemia (RBC's will be smaller)
hypochromic (too little color)
Vit B12 & Folic acid deficiency
Macrocytic anemia (bigger-can't divide normally and spend more time in growth phase)
megaloblastic macrocytic anemia
Lack of B12 b/c of lack of intrinsic factor (made by stomach, from same cells that make gastric acid)
Protects B12 from digestion: B12 needs to get through stomach to intestine for absorption
Cause: gastric mucosa destroyed via auto-immune mechanism)
-Elderly, Northern Europeans
-Testing: CBC test will show macrocytic, nomochromic anemia
-Cooking destroys it (green beens)
-Alcohol inhibits liver from mobilizing folic acid
-Pregnant women need supplements
O2 Capacity and O2 Content
"available seats in a room"
Amt of O2 that can be carried in blood assuming every heme has O2 bound to it
Hb (hemoglobin) carries 1.34 mL O2/100 mL blood
(100 mL=1 deciliter (1 dL) )
(1.34 mL O2/g Hb) (15 g Hb/dL blood)= 20.1 mL O2/dL blood=OXYGEN CAPACITY
O2 CONTENT: how much O2 is actually there. "150 people in a room"
-Need O2 % saturation (will be given)
Content=capacity x % saturation
=20.1 mL O2/dL x 95%= 19.1 mL O2/dL
*Normal O2 content=at least 90%
What is a symptom of low O2?
Where do RBC get ATP?
Via anaerobic glycolysis
They don't have mitochondria
*ATP needed for membrane flexibility, maintaine Fe 2+ state, prevent oxidation of Hb, ion transport (ATPase)
Glucose sticks to Hb
Fe in Hb
Iron (Fe) is recycled
Heme broken down to bilirubin
What can cause anemia?
↓ Hb content
Bone marrow damage (b/c no stem cells)
Kidney damage (loss of EPO)
Effects: too little O2
Too many RBC's (blood doping)
Effects: more O2 carrying content but thicker blood and heart thus has to work harder (blood is like honey)
Polycythemia vera (primary polycythemia)
-No EPO signal
-Bone marrow is making RBC when there isn't a need
Large amounts of Fe 3+ in blood is called what?
Sickle cell disease
RBC is deformed (hemoglobin defect)
Hb defect at AA#6 where valine(hydrophobic-wants to be on inside) is used instead of glutamic acid
Symptoms: pain, organ damage, strokes, ↑ infections
What affects Hb?
2,3-BPG =(altitude) reduces affinity (→ shift)
↓ pH=↓affinity (→ shift)
HbF (fetal) (fetus doesn't have binding site) ← shift
Anemia (you test for ferritin (not Fe)
Transport Fe in Enterocyte
1. Fe 3+→Fe 2+ via Dcytb
2. Into enterocyte via DMT1
3. On backside of cell, ferroportin sends it out of cell into blood via Hephestin → Fe 3+ → transferrin (Fe content is regulated by absorption via Hepcidin)
Pyridoxine responsive anemia
Proximal (bound to heme). Involved in changing conformation when O2 binds
Helps w/ signal or High or Low Fe
Organ dysfunction due to Fe overload: cirrhosis, arthritis, skin pigmentation
Genetic definition: classical HH
-Mutations in HFE gene (common mutation=C282Y)..involved in regulation of Fe absorption
-Regulated by Hfe
-Regulates export/import of Fe to bone marrow
-Binds to channel (ferroportin) that Fe goes through to get outside
-↑ hepcidin= ↓ferroportin = ↓Fe
Hfe and Hepcidin
Hfe controls Hepcidin
-If Hfe is mutation, it can't bind TFR2→can't turn on hepcidin expression → lots of ferroportin → Fe overdose