Chapter 19 Flashcards
(100 cards)
1
Q
cardiovascular system consists of **(3) interrelated components: **
A
- Blood
- Heart
- Blood vessels
2
Q
Blood
- **(3) **functions
A
1) Transportation- respiratory gases, nutrients & hormones to & from body’s cells.
2) Regulation- helps regulate body pH & temperature
3) Protection- clotting mechanisms & immune defenses
3
Q
Constituents of Blood
- characteristics of blood (3)
A
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)
4
Q
Amount of Blood
males vs. females
A
Blood Volume:
males = ~ 5-6 L
**females = ~ 4-5 L **
5
Q
If tube of anti-coagulated blood sits for period of time… what happens?
- Used for determining?
A
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
6
Q
Blood
A
liquid CT consisting of cells/cell fragments (formed elements) surrounded by liquid ECM **(blood plasma) **
7
Q
Formed Elements
** (3) principal components**
A
1) RBCs - bulk of blood
2) **WBCs **
3) Platelets (cell fragments)
8
Q
Types of WBCs (2)
A
1) Granular Leukocytes
a) neutrophils
b) eosinophils
c) basophils
2) Agranular Leukocytes
a) T & B lymphocutes & NK cells
b) Monocytes
9
Q
Hematocrit
A
% of total blood volume occupied by RBCs
10
Q
Hematocrit
males vs females
A
**males: **40-54%
**females: **38-46%
11
Q
Ratio of RBCs to WBCs
A
700 RBCs : 1 WBC
12
Q
Platelets
- abundance
- life span
- mass
- appearance
A
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
13
Q
Hemopoiesis/Hematopoiesis
- occurs in? (5)
A
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
14
Q
Erythropoiesis
A
part of hematopoiesis that deals with production of RBCs
15
Q
**Erythropoiesis **increases when?
A
states of **hypoxia **(O2 deficiency)
- stimulates kidneys to release hormone erythropoietin (EPO)
16
Q
Erythropoietin (EPO)
A
EPO circulates to red bone marrow
speeds up maturation & release of immature red cells
17
Q
RBCs
- shape
- characteristics
- function
A
bi-concave discs
- when mature, no nucleus or protein-making machinery
die in ~120 days
- carry O2 to tissues of body
18
Q
Functions of RBC shape
A
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
19
Q
Reticulocytes
A
immature RBCs
20
Q
Rate of **Erythropoiesis **
- measured by?
A
number of immature RBCs (reticulocytes) in peripheral circulation
21
Q
A low retic count
A
(<.5%) indicates low rate of erythropoiesis
22
Q
elevated rate
A
(>2%) indicates high rate of erythropoiesis
23
Q
Hemoglobin (Hgb)
A
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 **
24
Q
Each RBC contains __ ___ molecules of Hgb
A
280 million
25
Anemia
condition of **reduced oxygen carrying capacity** of blood due to **insufficient RBC’s** or **hemoglobin (quality/quantity)**
26
Anemia **is most often result of? (5)**
1. low iron intake
2. hemolysis
3. autoimmune disease
4. blood loss
5. lack of production in bone marrow
27
Polycythemia
condition of excess number of RBCs
28
Polycythemia **occurs in response to?**
1. **hypoxia** (natural “blood doping” = training at high altitude)
2. shots of **EPO** (illegal “doping”)
3. **smoking** (Chronic obstructive pulmonary disease- **COPD**)
4. **dehydration**
29
Types of Anemia (3)
1) Iron deficiency anemia
2) Hemorrhagic anemia
3) Sickle-cell disease (SCD) - sickle-cell anemia
30
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**
31
2) Hemorrhagic anemia
result of **precipitous blood loss** & results in equal decrease in **Hct**, **Hgb** content, and **RBC** count
32
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*
33
RBC life cycle
only 120 days
34
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*
35
**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**
36
Hemolysis
rupturing of **erythrocytes **(red blood cells)
37
WBCs
leukocytes
have nuclei & full complement of other organelles
- but they do not **Hemoglobin**
38
Function of **WBCs**
attack pathogens invading body
**lymphocytes** attack viruses
39
For diagnostic purposes, physicians measure ..
the total **number** of circulating **WBCs**
40
Leukocytosis
increased WBC count
**10,000/µL**
- usually indicate an **infection**, **surgery** or **strenuous** **exercise**
41
Leukopenia
decreased WBC count **(\< 5,000/µL) **
•usually indicates a **severe** **disease** (**AIDS**, **bone marrow failure**, severe **malnutrition**, or **chemotherapy**)
42
WBC differential
test that determines % of each of the **5 types of WBCs **
- to enhance diagnostic value of WBC count
-
43
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**)
44
Hemostatis
sequence of responses that stops bleeding
45
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
46
(3) mechanisms reduce **blood loss**
1) **vascular spasm**
2) formation of **platelet plug**
3) **blood clotting (coagulation)**
47
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
48
Vascular spasm
## Footnote
**caused by? (3) **
**damage** to smooth muscle
by **substances** **released** from **activated** **platelets**
by **reflexes** **initiated** by **pain** **receptors**.
49
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**
50
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
51
1) platelet adhesion
platelets **contact** & **stick** to parts of **damaged** **blood** **vessel** (**collagen** **fibers** of CT underlying damaged endothelial cells)
52
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
53
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**)
54
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
55
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
56
(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
57
(2) pathways to activate **clotting **
Intrinsic
Extrinsic
- lead to formation of **prothrombinase **
58
**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
-** once**CF X**is**activated**, combines with**factor V**in presence of Ca2+ to form **prothrombinase**
- initiates formation of **prothrombinase **
59
**Intrinsic **Pathway
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 **
60
Extrinsic Pathway
- speed, steps (general)
few steps
occurs rapidly
within seconds once protein **Tissue Factor (TF)** leaks into blood
61
Intrinsic Pathway
- steps, speed (general)
more complex
occurs more slowly
in response to damage to **endothelial cells **or **phospholipids **released by **activated platelets **
62
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)
63
Both **extrinsic** and **intrinsic** clotting pathways converge at ... where?
a **common point (pathway)** where **factor X** becomes **activated (Xa)**
64
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
65
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 **
66
Clot Retraction
consolidation of the fibrin clot
67
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**
68
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**.
69
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
70
**fibrinolytic system **
dissolves **small**, **inappropriate** clots
- also dissolves **clots** at a **site** of **damage** once damage is **repaired**
71
* *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)
72
Thrombosis
clotting in unbroken blood vessel (usually vein)
73
thrombus
clot
74
**Thrombus** may be initiated by?
**roughened** **endothelial** **surfaces** of a blood vessel resulting from
**atherosclerosis**, **trauma **or **infection →**induce adhesion of platelets
75
Embolus
when blood clot, air bubble, piece of fat or other debris is transported in blood stream
76
Embolus - dangerous?
In the worst circumstances (**pulmonary** **embolism** or **stroke**), **emboli** can obstruct
## Footnote
blood vessel & cause **ischemia** (restriction in blood supply) to tissue beds distal to obstruction
77
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
78
Intravascular clotting
- also form when?
when blood flows too **slowly (stasis) **
allows clotting factors to accumulate locally & initiate coagulation cascade
79
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*
80
Antigens
antibody generator
any substance which **provokes** an **adaptive** **immune** **response**
81
RBCs & antigens
RBCs have proteins on surface which act as **antigens (surface markers) **
82
Antigens within same species
not necessarily compatible with those of another
83
most significant of the 100 markers currently known to exist on RBCs
A and B antigens
84
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)
85
Antibodies & Antigens of blood
serum contains anti-ABO antibodies of type **opposite **to ABO antigen on red cell surface
86
Type AB
* *universal recipients **
- dont have Anti-A or Anti-B antibodies to destroy transfused RBCs
87
Type O
universal **donors**
RBCs have no antigens on cell surface to react with recipients serum
88
Agglutination
clumping of RBCs
**- antigen–antibody** response in which RBCs become **cross‐linked** to one another
89
•Agglutination with an antisera indicates?
presence of that **antigen** on the **RBC**
90
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
91
•Giving the wrong type blood can cause... (3)
the patient to develop a **fever**, serious **renal** **failure**, or go into **shock**.
92
Normally blood plasma contains or doesnt contain anti-Rh antibodies?
does NOT
93
Rh+
RBCs have Rh antigen
94
Rh-
lack Rh antigen
95
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+ **
96
**Hemolytic disease of the newborn (HDN) **results when?
when an Rh+ fetus develops in the womb of Rh- women
97
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*
98
Intravascular Clotting
blood clots form within cardiovascular system
initiated by roughened endothelial surfaces of blood vessels
99
Intravascular Clotting
Blood clots initiated by roughened endothelial surfaces of blood vessels resulting from? (3)
atherosclerosis
trauma
infection
100
