Blood Flashcards
1
Q
What type of tissue is blood?
A
connective
2
Q
Plasma
A
the nonliving liquid part
3
Q
Formed elements
A
- the living cells
- erythrocytes (RBCs), leukocytes (WBCs), thrombocytes (platelets)
4
Q
What is the average blood volume in men and women?
A
- men: 5.5 liters
- women: 5 liters
5
Q
Erythrocytes
A
- most common formed element
- 5 million RBCs in a cubic mm of blood
- trillions in the body
- packed with hemoglobin for O2 transport
6
Q
Hemoglobin (Hb)
A
- O2 loading in lungs (produces oxyhemoglobin)
- O2 unloading in tissues (produces deoxyhemoglobin or reduced hemoglobin)
- CO2 loading in tissues (20% of CO2 in blood binds to Hb- carbaminohemoglobin)
7
Q
Where are RBCs formed?
A
- in red bone marrow from hemocytoblasts or hematopoeitic stem cells
- control of production is based on O2 levels in blood
- in adults, kidney senses levels of O2
8
Q
Too few RBCs leads to…?
A
tissue hypoxia
9
Q
Too many RBCs…?
A
increases blood viscosity
10
Q
How many RBCs are made per second?
A
> 2 million RBCs made per second
11
Q
Balance between RBC production and
destruction depends on…?
A
- hormonal controls
- adequate supplies of iron, amino acids, and B vitamins
12
Q
Erythropoietin (EPO)
A
- if O2 levels are low (hypoxia), kidney releases erythropoietin (a hormone)
- stimulates the hematopoietic stem cells to become erythrocytes
- RBC count increase (due to prolonged exercise, high altitudes, and COPD)
- direct stimulus for erythropoiesis
- always small amount in blood to maintain basal rate (high RBCs or O2 levels depress production)
- dialysis patients have low RBC counts due to damaged kidneys
13
Q
Causes of hypoxia
A
- decreased RBC numbers due to hemorrhage or increased destruction
- insufficient hemoglobin per RBC (e.g., iron deficiency)
- reduced availability of O2 (e.g., high altitudes, consistent vigorous activity, COPD)
14
Q
How long do RBCs live?
A
- about 120 days
- old or damaged red blood cells
are removed by the spleen and the
liver - these are the most actively replaced
cells in the body
15
Q
What happens when RBCs are removed from blood?
A
- hemoglobin is broken down
into heme and globin - globin is a protein that is
digested and recycled - heme is broken down into iron
and bile pigments
16
Q
What happens to iron after heme is broken down?
A
- iron is stored in the liver and
transported back to the red bone
marrow as transferrin - bile pigments, biliverdin and bilirubin, are released into bile as waste and
ultimately end up in feces giving fecal
material its characteristic color
(brownish / greenish) - also gives urine its usual color
17
Q
Jaundice
A
- occurs when excess bile pigments
accumulate in body fluid and/or bile ducts are blocked, liver disease - sclera looks yellow and skin looks yellow in someone light-complected
- about 1/3rd of newborns have jaundice (liver needs time to mature; bili lights break down bile pigments)
18
Q
What are nutrient requirements for erythropoiesis?
A
nutrients, iron, vitamin B12, and folic acid
19
Q
Nutrients
A
amino acids, lipids, and
carbohydrates
20
Q
Iron
A
- available from diet
- 65% in Hb; rest in liver, spleen, and bone marrow
- free iron ions are toxic (stored in cells as ferritin and hemosiderin; transported in blood bound to protein transferrin)
21
Q
What is necessary for DNA synthesis for rapidly dividing cells?
A
Vitamin B12 and folic acid
22
Q
Anemia
A
- blood has abnormally low O2 carrying capacity
- sign rather than disease itself
- blood O2 levels cannot support normal metabolism
- accompanied by fatigue, pallor, shortness of breath, and chills
23
Q
Hemorrhagic anemia
A
- blood loss rapid (ex, stab wound)
- treated by blood replacement
24
Q
Chronic hemorrhagic anemia
A
- slight but persistent blood loss (hemorrhoids, bleeding ulcer)
- Primary problem treated
25
Q
Iron-deficiency anemia
A
- caused by hemorrhagic anemia, low iron intake, or impaired absorption
- iron supplements to treat
26
Q
Pernicious anemia
A
- autoimmune disease - destroys stomach mucosa
- lack of intrinsic factor needed to absorb B12 (deficiency in B12)
- RBCs cannot divide
- treated with B12 injections
- also caused by low dietary B12 (vegans)
27
Q
Renal anemia
A
- lack of EPO
- often accompanies renal disease
- treated with synthetic EPO
28
Q
Megaloblastic anemia
A
- larger, fragile RBCs
- usually caused by low folic acid
29
Q
Aplastic anemia
A
- destruction or inhibition of red marrow by drugs, chemicals, radiation, viruses
- sometimes all cell lines affected
- clotting and immunity defects
- treated short-term with transfusions
- long-term with transplanted stem cells, or synthetic erythropoietin (Procrit) if red marrow is okay, as in chemotherapy of metastatic cancer
30
Q
Sickle-cell anemia
A
- hemoglobin S (one amino acid wrong in a globin beta chain)
- RBCs crescent shaped when unload O2 or blood O2 low
- RBCs rupture easily and block small vessels (poor O2 delivery; pain)
31
Q
How does malaria affect sickle-cell anemia?
A
- two copies = sickle-cell anemia
- one copy = sickle-cell trait; milder disease; better chance to survive malaria (lower O2 levels inhibit the pathogen in the blood)
- Thalassemias (typically Mediterranean ancestry; helps with surviving malaria also)
32
Q
Polycythemia
A
- genetic predisposition or Bone marrow cancer - excess RBCs
- severely increased blood viscosity
- risk of blood clotting when not supposed to
33
Q
Secondary polycythemia
A
- less O2 available (high altitude) or EPO
production increases - higher RBC count - blood doping by athletes
34
Q
Leukocytes
A
- make up <1% of total blood volume
- function in defense against disease
- can leave capillaries via diapedesis (move through tissue spaces by ameboid motion and positive chemotaxis)
- 4,800 – 10,800 WBCs/μl blood
35
Q
Leukocytosis
A
- WBC count over 11,000/mm3
- normal response to infection
36
Q
What are the two categories of leukocytes?
A
granulocytes and agranulocytes
37
Q
Granulocytes
A
- visible cytoplasmic granules
- neutrophils, eosinophils, basophils
38
Q
Agranulocytes
A
- no visible cytoplasmic granules
- lymphocytes, monocytes
39
Q
Neutrophils
A
- most numerous WBCs
- also called Polymorphonuclear leukocytes (PMNs or polys)
- granules stain lilac; contain hydrolytic
enzymes - 3-6 lobes in nucleus; twice size of RBCs
- very phagocytic—”bacteria slayers”
- 55-70%
40
Q
Eosinophils
A
- red-staining granules
- bilobed nucleus
- granules lysosome-like
- release enzymes to digest parasitic worms
- role in allergies and asthma
- role in modulating immune response
- 1-4%
41
Q
Basophils
A
- rarest WBCs
- nucleus deep purple with 1-2 constrictions
- large, purplish-black (basophilic) granules contain histamine
- histamine: inflammatory chemical that acts as vasodilator to attract WBCs to inflamed sites
- are functionally similar to mast cells
- 0.5-1%
42
Q
Lymphocytes
A
- second most numerous WBC
- large, dark-purple, circular nuclei with thin rim of blue cytoplasm
- mostly in lymphoid tissue (e.g., lymph
nodes, spleen); few circulate in blood - crucial to immunity
- T lymphocytes and B lymphocytes
- 20-40%
43
Q
T Lymphocytes (T cells)
A
act against virus-infected cells and tumor cells
44
Q
B lymphocytes (B cells)
A
give rise to plasma cells, which produce antibodies
45
Q
Monocytes
A
- largest leukocytes
- abundant pale-blue cytoplasm
- dark purple-staining, U- or kidney-shaped nuclei
- leave circulation, enter tissues, and
differentiate into macrophages - 2-8%
46
Q
Macrophages
A
-actively phagocytic cells
- crucial against viruses, intracellular bacterial parasites, and chronic infections
47
Q
Leukopenia
A
abnormally low WBC count—drug induced
48
Q
Leukemias
A
- all fatal if untreated
- cancer - overproduction of abnormal WBCs
- named according to abnormal WBC clone involved
- acute leukemia derives from stem cells; primarily affects children
- chronic leukemia more prevalent in older people
49
Q
A
