Ch.17 Flashcards
(66 cards)
1
Q
Characteristics of Blood
KNOW
A
- Connective tissue
- pH 7.35-7.45
- temp. 100.4 F, 38 C
- 5X more viscous than water
- Color depends on the amount of oxygen – bright red to maroon
- Average volume for adult males – 5 to 6 L (1.5 gal); for adult females – 4 to 5 L
2
Q
Functions of Blood
KNOW
A
- Distribution – O2, CO2, nutrients, wastes,
hormones, etc. - Regulation - blood pH, temp. homeostasis
- Protection - circulates platelets, WBC’s and other proteins for immunity and clotting
3
Q
Two Components of blood
A
- Plasma = liquid portion
- Formed elements = cells and cell fragments
- Buffy coat: leukocytes and platelets
- Erythrocytes
4
Q
Plasma composition
A
- 8% Proteins Solutes
- Albumin
- Globulins
- Fibrinogen - 90% Water
- Non-Protein Solutes
- Electrolytes
- Nutrients
- Gases
- Hormones
- Waste
5
Q
Albumin
A
- 60% of plasma proteins
- main contributor to osmotic pressure (pressure that helps to keep water in blood circulation)
- shuttles molecules thru circulation acts as a buffer in blood
- Increase albumin -> incr water in blood -> incr blood volume -> incr blood pressure
6
Q
Red Blood Cells (RBC’s), White Blood Cells (WBC’s), Platelets
A
All made continuously in
the bone marrow and most
have a short life span
7
Q
Hematopoiesis
A
- produces red blood cells/erythrocytes
- occurs in the red bone marrow
- hematopoietic stem cell > reticulocyte > RBC/erythrocyte
- reticulocyte is young RBC/erythrocyte and indicate an estimate of rate of RBC formation
- RBC’s and platelet numbers remain relatively constant (due to negative feedback systems), but WBC’s numbers fluctuate depending on presences of antigens
8
Q
Complete Blood Count
A
- RBCs: total, HCT (amount of space RBCs take in blood), Hb, & RBC indices
- Platelet count
- WBCs: total number & differential (number of each type)
9
Q
Hematocrit/HCT
A
% of blood volume occupied by RBC’s, normal = 42 to 52% males (higher vs. females due to testosterone); 37 to 47 % females (some loss due to menstruation)
10
Q
Interesting factoids
A
- 1 drop of blood contains about 250,000,000 RBC’s
- You make new RBC’s at a rate of 2 million/second and about the same amount are destroyed/second in the liver, spleen, and bone marrow – the parts are recycled
- too many RBC’s (polycythemia) and blood gets sticky > resists flow
- too few RBC’s (anemia) results in hypoxia (lack of oxygen to the tissues)
11
Q
3 red blood cell indices
A
- mean corpuscular volume (MCV): shows the size of the red blood cells.
- mean corpuscular hemoglobin (MCH): amount of hemoglobin in an average red blood cell.
- Mean corpuscular hemoglobin concentration (MCHC): the ratio of amount of hemoglobin per cell per unit of volume of the cell – chromicity (more Hb, normochromic = rosier & ruddier vs hypochromic cell is pale with little Hb).
- These numbers help in the diagnosis of different types of anemia. Red cell distribution width (RDW) can also be measured which shows if the cells are all the same or different sizes or shapes.
12
Q
Red blood cell Structure
KNOW
A
- small, biconcave disk shaped cells (more surface area = better for diffusion)
- also known as erythrocytes.
- No nucleus, no mitochondria and few of other organelles
- sacs of hemoglobin (about 280 million hemoglobin molecules per RBC)
- live ~ 120 days; during that time it travels through the body about 75,000 times
13
Q
Hemoglobin (Hb/Hgb)
RBC Structure
A
- is made of 4 peptide chains (2 alpha & 2 beta)
- each chain has a heme group associated with it
- each heme group has an iron (so 4 fe2+/hemoglobin)
- each iron can bind reversibly with 1 O2 molecule
- each RBC’s has 250 million hemoglobin molecules
- Carbon dioxide can also be carried by hemoglobin and binds to amino acid region (NOT the heme group) … carbaminohemoglobin (from tissues to lungs)
14
Q
Oxyhemoglobin
RBC Structure
A
- ruby red
- travels from lungs to tissues
15
Q
Deoxyhemoglobin
A
- maroon
- at tissues after O2 is released
16
Q
Hb Values
A
Normal hemoglobin values for
- adult males: 13 to 18 g/100 ml
- adult females: 12-16 g/100 ml
- infants: 14 – 20 g/100 ml
17
Q
Fate and Destruction of RBCs
A
- RBCs can’t make new proteins as they have no nucleus
- Dying erythrocytes engulfed by macrophages
- Iron stored as ferritin
- Heme group degraded to bilirubin
- Iron is transported in blood by transferrin
18
Q
Anemia
KNOW
A
- inadequate supply of oxygen to tissues
- symptoms = fatigue, pale, short of breath, chills
- causes:
1. insufficient number of RBC’s due to hemorrhage, infections that cause hemolysis, lack of components to make RBC’s, or slow rate of cell production (low EPO); destruction of marrow (pernicious anemia – lack B12 to do mitosis)
2. Decrease in amount of hemoglobin due to lack of iron
3. Abnormal hemoglobin due to genetic disease such as sickle cell anemia or thalassemia
19
Q
Hemorrhagic anemia
KNOW
A
due to severe blood loss
20
Q
Pernicious anemia
KNOW
A
due to lack of vitamin B12 (usually due to lack of intrinsic factor production by stomach)
21
Q
Sickle-cell anemia
KNOW
A
- due to misshapen RBCs
- dam-up -> pain, stroke
- RBCs rupture easily, infection
22
Q
Iron-deficiency anemia
KNOW
A
secondary to hemorrhagic anemia
23
Q
Renal anemia
KNOW
A
lack of EPO (leads to erythropoietin release by kidneys in response to HYPOXIA; ex: recent move to higher altitude)
24
Q
Aplastic anemia
KNOW
A
from destruction or inhibition of red marrow
25
EPO Mech for Erythropoiesis
| Homeostasis: Normal blood oxygen levels
1. Stimulus: Hypoxia (inadequate O2 delivery) due to decreased RBC count and decreased ability of O2
2. kidney (and liver) releases erythropoietin
3. erythropoietin stimulates red bone marrow
4. enhanced erythropoiesis increases RBC count
5. Response: Oxygen carrying ability of the blood
26
Pernicious anemia
- autoimmune disease
- B complex vitamins, B12 and folic acid, are required for DNA synthesis, so they are necessary for cells undergoing lots of cell division (bone marrow)
- Lack of B12 usually due to a disorder in the stomach lining, as parietal cells in the stomach secrete a substance called intrinsic factor required to absorb B12
27
Anemia and vitamin C
- Vitamin C increases absorption of iron in the digestive tract
- Drinking orange juice with a meal is a good way to boost iron intake
- Drinking tea with a meal reduces absorption of iron because tannic acid in tea binds with the iron and prevents its absorption
- Poor vitamin C = lower iron
28
Hemolytic Anemias
- General causes: Transfusion of mismatched blood; bacterial or parasitic infection
29
Thalassemias
| Hemolytic Anemia
typically seen in people of Mediterranean ancestry (Greeks and Italians). Many subtypes of thalassemias, classified according to which hemoglobin chain is affected. Range in severity from mild to severe which require monthly blood transfusions.
30
Sickle Cell Anemia
| Hemolytic Anemia
- RBCs crescent shape due to one faulty amino acid in the hemoglobin chain of 146 amino acids
- erythrocytes rupture easily and tend to dam up in small blood vessels. Leaves victims in severe pain.
- As the spleen works harder to recycle the too short lived RBCs, infection becomes more likely. Most victims receive antibiotics prophylactically. Strokes are also more common. Occurs in 1 in 500 black newborns in the U.S.
31
Polycythemia
- too many RBC’s (sluggish blood)
- Due to bone marrow cancer, change in altitude, or use of synthetic erythropoietin
- Ex: Polycythemia vera (bone marrow cancer) possible Hct 80%
32
Secondary Polycythemia
- Stimulated by HYPOXIA (low O2 in blood -> stimulates kidneys to produce EPO), as less oxygen is available
- Natural response to people who live at high altitudes (mountains) as higher altitudes have lower atmospheric pressure (less oxygen)
- Results in higher RBC counts
- Will reverse as the person returns to lower altitude
33
Blood Doping /Artificial Secondary Polycythemia
- Aerobic athlete practice of artificially-induced polycythemia
- Subject to negative effects: stroke, heart failure via high blood viscosity/Hct
- RBC’s removed, stored, then reinjected after EPO has already stimulated RBC replacement… better oxygen delivery -> endurance -> speed
34
White Blood Cells (Leukocytes)
- Have nucleus and other normal organelles
- Account for less than 1% of blood volume
- About 4,800 to 10,800 per microliter of blood
- Have chemical arsenals for defense
- Recognize self from non-self
- Chemotaxis (migrate to areas of tissue damage or infection via chemical trail released by damaged cells or other leukocytes) and Diapedesis (leave blood vessels)
- Leukocytosis – WBC > 11,000; indicates bacterial or viral infection
35
Granulocytes
| Classification of WBC
- larger than RBC’s, have granules packed with chemical arsenals/some granules are defensins (antimicrobial proteins)
- types:
1. Neutrophils
2. Eosinophils
3. Basophils (in blood)
36
Neutrophils
| White blood cell > Granulocytes > Neutrophils
- 50-70%
- also called polymorph (nucleus has various numbers of lobes)
- Granules stain pale lilac
- phagocytes (cell-eating)
- usually first to arrive at an infection
- increase numbers during bacterial and fungal infections, appendicitis and meningitis, inflammation and stress
- Defensins work via poking holes in membrane of invaders’ cells
- Neutrophils are a.k.a. polymorphonuclear leukocytes / PMN’s (nucleus with differing number of lobes)
- Utilize “respiratory burst” – metabolize oxygen to H2O2 & bleach to kill cells
37
Eosinophils
| White blood cell > Granulocytes > Eosinophils
- 2-4%
- fight parasitic worms
- Granules stain bright red
- Degranulate to kill parasites too large to phagocytose
38
Basophils (in blood)
| White blood cell > Granulocytes > Basophils
## Footnote
KNOW
- 0.5- 1%
- Granules stain purplish black
- release histamine that causes
- allergic reactions & heparin; similar to mast cells ( in tissue); participate in anaphylaxis
- Mast cells & basophils both bind IgE (immunoglobulin E) -> histamine granules are released from mast cells & basophils
39
Lymphocytes
| Agranulocytes > Lymphocytes
## Footnote
KNOW
- 25%
- Large dark purple nucleus that occupies most of the cell
- Most reside in lymphatic tissue, some circulate in blood
- T cells for cell mediated immunity
- B cells (Plasma Cells) for antibody mediated immunity (or humoral immunity)
40
Monocytes
| Agranulocytes > Monocytes
## Footnote
KNOW
- 3-8%
- phagocytes
- when leave circulatory system are called macrophages
- Increase in viral and bacterial infections, and some chronic diseases
- Largest blood cell
- Activate other lymphocytes to activate the immune response
41
Leukocytosis
- too many WBC’s > nonfunctional
- Leukemia = cancer of WBC’s
42
Mononucleosis
viral infection during which you accumulate nonfunctional agranulocytes
43
Leukopenia
- too few WBC’s
- Usually drug induced (particularly anticancer drugs and glucocorticoid hormones) + radiation therapy
44
Leukopoiesis
- production of WBC’s stimulated by chemical messengers: ILs & CSFs
- Chemicals (hormones) stimulate: ex = interleukins (ILs) & colony-stimulating factors (CSFs)
- CSFs are named for the type of WBC they stimulate (ex: g-CSF stimulates granulocytes)
- All originate from hematopoietic stem cell (hemocytoblast), same as with RBC production
45
Platelets (thrombocytes)
- Not true cells, just cell fragments (1 megakaryoblast split into 2000-3000 platelets)
- Age quickly because they are anucleate; degenerate in about 10 days
- contain enzymes + granules with clotting proteins
- Formation regulated by thrombopoietin
46
Hemostasis
sequence of events that stops
bleeding (prevent hemorrhage) in small vessels
47
3 steps in blood clotting
1. vascular spasm
- damage to vessel walls causes vascular smooth muscle to contract to form temporary seal (can reduce blood loss for typically 20-30 minutes)
- also results in release of chemical signals from endothelial cells & platelets
2. platelet plug
- Platelet adhesion w/ injury: collagen from walls is exposed > platelets stick to the wall > swell and form spiky processes(w/o injury, NO & PG prevent platelet aggregation)
- Release reaction (degranulation):
-- serotonin & thromboxane A2: enhances smooth muscle contraction & attracts platelets -- ADP: attracts more platelets to the area
- Platelet Aggregation: positive feedback loop more platelets adhere to form a temporary plug
3. coagulation
- blood changes from liquid to gel at the plug site (note: actually requires ~30 clotting factors made by platelets, endothelial cells, & liver that circulate in inactive form + calcium ions)
- FIBRIN “glues” aggregation of platelets
1. formation of prothrombin activator
by intrinsic or extrinsic mechanism
2. prothrombin → thrombin (activated enzyme)
3. fibrogen (soluble) → fibrin (insoluble)
4. mesh clot
48
Clot Retraction
| Hemostasis
Actin and myosin in platelets contract to bring edges of vessels together (30-60 min after injury)
49
Vessel Repair
| Hemostasis
Platelet Derived growth Factor (PDGF) stimulates vessel repair (produced by platelets) via fibroblasts forming a connective tissue patch
50
Fibrinolysis
- dissolving the clot… AFTER tissue has been repaired (begins about 2 days after injury)
1. Plasminogen activator (secreted by endothelial cells)
2. plasminogen → plasmin
3. plasmin dissolves clot
51
Intrinsic pathway of blood clotting
- factors needed for clotting are present in blood in inactive form all the time, just become activated to participate in clot production
52
Extrinsic pathway of blood clotting
TF is only clotting factor not normally present in blood
53
Factors Limiting Normal Clot Growth
- Antithrombin III: protein normally present in plasma; inactivates circulating thrombin (not attached to clot/fibrin)
- Protein C: inhibits CF pathways
- Heparin: found in basophil & mast cell granules; inhibits thrombin via enhancing antithrombin III; inhibits CF pathways; also found on surface of endothelial cells
- CF=clotting factors
54
Thrombus
| Clotting Disorder
- clots stuck to wall
- May block blood circulation and tissue will not get oxygen
55
Embolus
| Clotting Disorder
clot breaks away from wall and circulates until it gets to a smaller vessel and then blocks the vessel; can cause strokes (blocks bv @ brain), heart attack (blocks bv @ heart), pulmonary embolism (blocks bv @ airway)
56
Anticoagulant drugs
- prevent undesirable clotting
- Aspirin (blocks platelet aggregation & plug formation) – can help prevent heart attack
- Warfarin (Coumadin) (interferes with production of some clotting factors – reduces risk of stroke)
57
Thrombocytopenia
| Bleeding Disorder
- lack of sufficient circulating platelets
- Causes petechiae on the skin due to spontaneous bleeding of skin capillaries
58
Liver disease
| Bleeding Disorder
lack of clotting factors required for clotting
59
Hemophilia
| Bleeding Disorder
sex-linked genetic disorder lack of instruction to make clotting factors
60
Transfusions
- Blood losses of 15 to 30% cause pallor and weakness
- Loss of more than 30% of blood volume results in severe shock and death
- Whole blood transfusions – when blood loss is rapid and substantial
- Packed RBC (whole blood with plasma removed) used to restore oxygen carrying capabilities
- Shelf life of collected blood is 35 days at 4 C. Blood is usually separated into components to be used as needed.
61
Blood groups
- There are many groups of antigens on RBC membranes
- Within each group there are several naturally occurring genetic variations (types)
- ABO and Rh groups are important enough to cause transfusion reactions
- RBC surface antigens promote agglutination so a.k.a. agglutinogens
- ABO groups are based on presence or absence of agglutinogens: type A and type B
- Agglutinins: antibodies in plasma that act on RBCs with agglutinogens NOT present on person’s own RBCs
62
Type A
Agglutinogen: A Antigen
Agglutinin: Anti-B antibody
Blood type that can be received: A, O
63
Type B
Agglutinogen: B Antigen
Agglutinin: Anti-A antibody
Blood type that can be received: B, O
64
Type AB
Agglutinogen: A and B antigens
Agglutinin: no antibody
Blood type that can be received: A, B, AB, O
Universal RECIPIENT
65
Type O
Agglutinogen: neither A and B antigen
Agglutinin: anti-A and anti-B antigen
Blood type that can be received: O, Universal DONOR
66
Hemolytic disease of newborn / erythroblastosis fetalis
- A Rh- mom will be given RhoGAM before or shortly after she gives birth to her Rh+ baby. RhoGAM contains anti-Rh agglutinins (agglutinates the Rh factor to block mom’s development of Rh antibodies)
- If the mom is not treated & becomes pregnant with another Rh+ baby, her antibodies will cross the placenta & destroy baby’s RBCs -> hemolytic disease of the new born / erythroblastosis fetalis
