Blood Flashcards
(34 cards)
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
Hematocrit=% of blood that is cells
normal: men=40-50%
women=35-45%
-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)
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)
B12 deficiency
Pernicious anemia
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
Folate
- 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) )
SO……
(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?
Confusion
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)
Hb A1C=
Glucose sticks to Hb
Fe in Hb
Iron (Fe) is recycled
Heme broken down to bilirubin
What can cause anemia?
↓ RBC ↓ Hb content ↓ Folate/B12 ↓ Fe Bone marrow damage (b/c no stem cells) Kidney damage (loss of EPO)
Effects: too little O2
Polycythemia
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?
methemoglobinemia
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
-Hemolytic anemia
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
Fe deficiency
Anemia (you test for ferritin (not Fe)
- poor diet
- menstruation
- hypochromic microcytic
Treatment: supplements
Fe 3+=damage
Transport Fe in Enterocyte
- Fe 3+→Fe 2+ via Dcytb
- Into enterocyte via DMT1
- 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
B6 deficiency
