Chapter 19 Flashcards
cardiovascular system consists of **(3) interrelated components: **
- Blood
- Heart
- Blood vessels
Blood
- **(3) **functions
1) Transportation- respiratory gases, nutrients & hormones to & from body’s cells.
2) Regulation- helps regulate body pH & temperature
3) Protection- clotting mechanisms & immune defenses
Constituents of Blood
- characteristics of blood (3)
CT cells (45%)
suspended in **blood plasma - **salt-water-&-protein solution **(55%) **
**- viscous **(thick)
- more **dense **than water
- slightly alkaline pH (7.35-7.45)
Amount of Blood
males vs. females
Blood Volume:
males = ~ 5-6 L
**females = ~ 4-5 L **
If tube of anti-coagulated blood sits for period of time… what happens?
- Used for determining?
cellular portion (RBCs) will precipitate out of soln & form heavier sediment below the straw colored liquid plasma
**- buffy coat **(WBCs & platelets) between
- Used for determining a persons hydration level
Blood
liquid CT consisting of cells/cell fragments (formed elements) surrounded by liquid ECM **(blood plasma) **
Formed Elements
** (3) principal components**
1) RBCs - bulk of blood
2) **WBCs **
3) Platelets (cell fragments)
Types of WBCs (2)
1) Granular Leukocytes
a) neutrophils
b) eosinophils
c) basophils
2) Agranular Leukocytes
a) T & B lymphocutes & NK cells
b) Monocytes
Hematocrit
% of total blood volume occupied by RBCs
Hematocrit
males vs females
**males: **40-54%
**females: **38-46%
Ratio of RBCs to WBCs
700 RBCs : 1 WBC
Platelets
- abundance
- life span
- mass
- appearance
megakaryote fragments
- more numerous than WBCs (150-400 x 103/mm3 )
- short life span (5-9 days)
- don’t have much mass
appear as little specks (no nucleus) interspersed among many red cells
Their granules contain chemicals that promote blood clotting once released
Hemopoiesis/Hematopoiesis
- occurs in? (5)
process by which formed elements of blood develop
- occurs in **embryo yolk sac, liver, spleen, thymus of fetus, red bone marrow **just before birth & throughout life
Erythropoiesis
part of hematopoiesis that deals with production of RBCs
**Erythropoiesis **increases when?
states of **hypoxia **(O2 deficiency)
- stimulates kidneys to release hormone erythropoietin (EPO)
Erythropoietin (EPO)
EPO circulates to red bone marrow
speeds up maturation & release of immature red cells
RBCs
- shape
- characteristics
- function
bi-concave discs
- when mature, no nucleus or protein-making machinery
die in ~120 days
- carry O2 to tissues of body
Functions of RBC shape
Characteristic RBC shape:
increases cell surface area & gives high oxygen carrying capacity
**- lack mitochondria **so dont use O2 they carry
- produce ATP anaerobically*
- allows them to deform, fit in small capillary beds & squeeze through narrow channels in spleen & capillaries
Reticulocytes
immature RBCs
Rate of **Erythropoiesis **
- measured by?
number of immature RBCs (reticulocytes) in peripheral circulation
A low retic count
(<.5%) indicates low rate of erythropoiesis
elevated rate
(>2%) indicates high rate of erythropoiesis
Hemoglobin (Hgb)
protein molecule adapted to carry O2 (& CO2)
- consists of 4 large globin proteins (2 alpha & 2 beta chains)
- each embedding an **iron-containing heme center **
Each RBC contains __ ___ molecules of Hgb
280 million
Anemia
condition of reduced oxygen carrying capacity of blood due to insufficient RBC’s or hemoglobin (quality/quantity)
Anemia is most often result of? (5)
- low iron intake
- hemolysis
- autoimmune disease
- blood loss
- lack of production in bone marrow
Polycythemia
condition of excess number of RBCs
Polycythemia occurs in response to?
- hypoxia (natural “blood doping” = training at high altitude)
- shots of EPO (illegal “doping”)
- smoking (Chronic obstructive pulmonary disease- COPD)
- dehydration
Types of Anemia (3)
1) Iron deficiency anemia
2) Hemorrhagic anemia
3) Sickle-cell disease (SCD) - sickle-cell anemia
1) Iron deficiency anemia
most common anemia in U.S.,
- affects primarily menstruating women
In the US, 20% of all women of childbearing age have iron deficiency anemia compared with only 2% of adult men
2) Hemorrhagic anemia
result of precipitous blood loss & results in equal decrease in Hct, Hgb content, and RBC count
3) Sickle-cell disease (SCD) - sickle-cell anemia
= autosomal recessive disorder
- genetic defect in primary DNA sequence leads to production of faulty Hgb & RBCs that take on a rigid, sickle-shape
- Sickling decreases cells’ flexibility increasing chance of rupture
- Erythropoiesis cannot keep up with hemolysis, leading to anemia
RBC life cycle
only 120 days
To maintain normal numbers of RBCs…
new mature cells must enter circulation at rate of at least 2 million/second
- pace that balances rate of RBC destruction*
Ruptured RBCs - what happens to them?
removed from circulation & destroyed by macrophages in spleen, liver & red bone marrow
—breakdown products are recycled & used in numerous metabolic processes, including formation of new RBCs
Hemolysis
rupturing of **erythrocytes **(red blood cells)
WBCs
leukocytes
have nuclei & full complement of other organelles
- but they do not Hemoglobin
Function of WBCs
attack pathogens invading body
lymphocytes attack viruses
For diagnostic purposes, physicians measure ..
the total number of circulating WBCs
Leukocytosis
increased WBC count
10,000/µL
- usually indicate an infection, surgery or strenuous exercise
Leukopenia
decreased WBC count **(< 5,000/µL) **
•usually indicates a severe disease (AIDS, bone marrow failure, severe malnutrition, or chemotherapy)
WBC differential
test that determines % of each of the **5 types of WBCs **
- to enhance diagnostic value of WBC count
-
Shifts in the normal percentages of circulating WBCs will often point towards? (2)
bacterial infection (elevated % of neutrophils)
or
a viral infection (elevated % of lymphocytes)
Hemostatis
sequence of responses that stops bleeding
When blood vessels are damaged/ruptured, the hemostatic response must be… (3)
quick
localized to region of damage
carefully controlled in order to be effective
(3) mechanisms reduce blood loss
1) vascular spasm
2) formation of platelet plug
3) blood clotting (coagulation)
1) Vascular spasm
When arteries/arterioles are damaged, circularly arranged smooth muscle in walls contracts immediately (reaction called vascular spasm)
- reduces blood loss for minutes to hours - during which other hemostatic mechanisms operate
Vascular spasm
**caused by? (3) **
damage to smooth muscle
by substances released from activated platelets
by reflexes initiated by pain receptors.
2) Platelet plug
- (3) steps
Platelets store many chemicals
- within vesicles are clotting factors, ADP, ATP, Ca2+ & serotonin
- also have **platelet derived growth factor (PDGF) **
1) platelet adhesion
2) platelet release rxn
3) platelet aggregation
platelet derived growth factor (PDGF)
hormone that can cause proliferation of vascular endothelial cells, vascular smooth muscle fibers & fibroblasts to help repair damaged blood vessel walls
1) platelet adhesion
platelets contact & stick to parts of damaged blood vessel (collagen fibers of CT underlying damaged endothelial cells)
2) platelet release rxn
due to adhesion, platelets activated
extend projections that allow them to contact & interact with each other
- begin to liberate contents of vesicles - **platelet release rxn **
Liberated ADP & Thromboxane A2 activate nearby platelets
**Seratonin & Thromboxane A2 **= vasoconstrictors - cause/sustain contraction of vascular smooth muscle to decrease blood flow through injured blood vessel
3) platelet aggregation
release of ADP makes other platelets sticky
- causing them to adhere to originally activated platelets
- **platelet aggregation **
eventually, accumulation & attachment of large #s of platelets form mass (platelet plug)
Clotting (coagulation)
series of enzymatic rxns in which each clotting factor activates many molecules of next one in fixed sequence
- finishes in formation of **fibrin threads **
involves **clotting factors **(Ca2+, inactive enzymes (synthesized by hepatocytes) & other molecules associated with platelets
(2) pathways to activate
Clotting (coagulation) is possible because of?
occurs in?
presence of several clotting proteins normally dissolved (soluble) in the blood
- once activated, soluble clotting factors become insoluble
cascading fashion where one activated clotting protein triggers next & so on
(3) stages of clotting
1) extrinsic/intrinsic pathway - forms prothrombinase
2) **prothrombinase **converts **prothrombin **(plasma protein formed by liver) into enzyme thrombin
3) **thrombin **converts soluble **fibrinogen **(another plasma protein formed by liver) into insoluble fibrin - forms threads of clot
(2) pathways to activate **clotting **
Intrinsic
Extrinsic
- lead to formation of **prothrombinase **
Extrinsic Pathway
**Tissue Factor (TF) **or **thromboplastin **leaks into blood from cells outside blood vessels
- complex mix of lipoproteins & phospholipids released from surfaces of damaged cells
In presence of Ca2+, TF begins sequence of rxns that ultimately activates clotting factor X
- onceCF Xisactivated, combines withfactor Vin presence of Ca2+ to form prothrombinase
- initiates formation of **prothrombinase **
**Intrinsic **Pathway
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activators in direct contact with blood or contained within blood
If endothelial cells roughened/damaged, blood contacts collagen in CT around blood vessel endothelium
- damage to platelets - release of **phospholipids **
**contact with collagen **or **glass **activates clotting factor **XII - **sequence of rxns eventually activate clotting factor **X **
**- **platelet phospholipids & Ca2+ also participate in activation of factor X
activated factor **X **combines with factor **V **to form **prothrombinase **
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Extrinsic Pathway
- speed, steps (general)
few steps
occurs rapidly
within seconds once protein Tissue Factor (TF) leaks into blood
Intrinsic Pathway
- steps, speed (general)
more complex
occurs more slowly
in response to damage to **endothelial cells **or **phospholipids **released by **activated platelets **
Common Pathway
Prothrombinase converts prothrombin (plasma protein formed by liver) into enzyme thrombin.
Thrombin converts soluble fibrinogen (another plasma protein formed by liver) into insoluble fibrin (forms threads of clot)
Both extrinsic and intrinsic clotting pathways converge at … where?
a common point (pathway) where factor X becomes activated (Xa)
Common Pathway - detailed
Prothrombinase + Ca2+ catalyze conversion of prothrombin to thrombin
Thrombin (in presence of Ca2+) converts soluble fibrinogen to insoluble fibrin threads
- also activates factor **XIII **(fibrin stabilizing factor) - strengthens/stabilizes fibrin threads into sturdy clot
Thrombin has **(2) positive feedback effects. **
1) involves factor V
- accelerates formation of **prothrombinase **- accelerates production of more **thrombin **
2) **thrombin **activates **platelets **which reinforces aggregation & release of **platelet phospholipids **
Clot Retraction
consolidation of the fibrin clot
Clot Retraction - process
As clot retracts as platelets pull on fibers, it pulls edges of damaged vessel closer together,
decreasing risk of further damage
– new endothelial cells can then repair the vessel lining
Normal retraction depends on?
adequate number of platelets in clot
- which release factor XIII & other factors, *thereby strengthening and stabilizing clot. *
- *fibroblasts form CT **in ruptured area & new endothelial cells repair vessel lining.
Because blood clotting involves amplification & positive feedback cycles, a clot has a tendency to? creating the potential for?
enlarge
impairment of blood flow through undamaged vessels
**fibrinolytic system **
dissolves small, inappropriate clots
- also dissolves clots at a site of damage once damage is repaired
- *FIbrinolysis**
- process
When clot is formed, inactive plasma enzyme **plasminogen **is incorporated into clot
both body tissues & blood contain substances that can activate **plasminogen **to become **plasmin - **enzyme that dissolves clots
(by digesting fibrin threads &inactivating substances such as fibrinogen, prothrombin & factors V and XII)
Thrombosis
clotting in unbroken blood vessel (usually vein)
thrombus
clot
Thrombus may be initiated by?
roughened endothelial surfaces of a blood vessel resulting from
atherosclerosis, **trauma **or infection →induce adhesion of platelets
Embolus
when blood clot, air bubble, piece of fat or other debris is transported in blood stream
Embolus - dangerous?
In the worst circumstances (pulmonary embolism or stroke), emboli can obstruct
blood vessel & cause ischemia (restriction in blood supply) to tissue beds distal to obstruction
Atherosclerosis
plaque builds up inside arteries - forms rough surface - activates factors
artery wall thickens as a result of invasion and accumulation of white blood cells
Intravascular clotting
- also form when?
when blood flows too **slowly (stasis) **
allows clotting factors to accumulate locally & initiate coagulation cascade
Important factors that inhibit thrombosis
undamaged blood vessels with smooth surfaces
good circulation
non-sticky platelets
- administration of anticoagulants & platelet inhibiting drugs (aspirin-like) - can reverse thrombus formed
Antigens
antibody generator
any substance which provokes an adaptive immune response
RBCs & antigens
RBCs have proteins on surface which act as **antigens (surface markers) **
Antigens within same species
not necessarily compatible with those of another
most significant of the 100 markers currently known to exist on RBCs
A and B antigens
basis of ABO blood group system
presence/absence of **A & B red cell antigens **
- Rh antigen: another major red cell antigen (85% of popn have)
Antibodies & Antigens of blood
serum contains anti-ABO antibodies of type **opposite **to ABO antigen on red cell surface
Type AB
- *universal recipients **
- dont have Anti-A or Anti-B antibodies to destroy transfused RBCs
Type O
universal donors
RBCs have no antigens on cell surface to react with recipients serum
Agglutination
clumping of RBCs
- antigen–antibody response in which RBCs become cross‐linked to one another
•Agglutination with an antisera indicates?
presence of that antigen on the RBC
vIn a blood transfusion, if the recipient receives the wrong blood type.. what happens?
** antigen-antibody reactions** will cause a rapid destruction (hemolysis) of donor red blood cells
•Giving the wrong type blood can cause… (3)
the patient to develop a fever, serious renal failure, or go into shock.
Normally blood plasma contains or doesnt contain anti-Rh antibodies?
does NOT
Rh+
RBCs have Rh antigen
Rh-
lack Rh antigen
Rh incompatibility - mother & child
If blood from Rh+ fetus sensitizes Rh- mother during birth, anti-Rh antibodies will form in the blood of that woman.
During next pregnancy anti-Rh antibodies can cross placenta to affect next baby if it is **Rh+ **
**Hemolytic disease of the newborn (HDN) **results when?
when an Rh+ fetus develops in the womb of Rh- women
To prevent HDN
Rh- mothers are given injection of RhoGAM (commercially produced anti-Rh antibody)
– at various points in her pregnancy (just before and after delivery)
•administered RhoGAM destroys any Rh+ antigens from baby before mother’s immune system can become sensitized to them & produce her own anti-Rh antibody.
For this same reason, RhoGAM is given to Rh- patients who have abortions/miscarriages
Intravascular Clotting
blood clots form within cardiovascular system
initiated by roughened endothelial surfaces of blood vessels
Intravascular Clotting
Blood clots initiated by roughened endothelial surfaces of blood vessels resulting from? (3)
atherosclerosis
trauma
infection
