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KIN 267 > Chapter 19 > Flashcards

Chapter 19 Flashcards

1
Q

cardiovascular system consists of **(3) interrelated components: **

A
  1. Blood
  2. Heart
  3. Blood vessels
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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

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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)
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4
Q

Amount of Blood

males vs. females

A

Blood Volume:

males = ~ 5-6 L

**females = ~ 4-5 L **

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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
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6
Q

Blood

A

liquid CT consisting of cells/cell fragments (formed elements) surrounded by liquid ECM **(blood plasma) **

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7
Q

Formed Elements

** (3) principal components**

A

1) RBCs - bulk of blood
2) **WBCs **
3) Platelets (cell fragments)

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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

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9
Q

Hematocrit

A

% of total blood volume occupied by RBCs

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10
Q

Hematocrit

males vs females

A

**males: **40-54%

**females: **38-46%

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11
Q

Ratio of RBCs to WBCs

A

700 RBCs : 1 WBC

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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

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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
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14
Q

Erythropoiesis

A

part of hematopoiesis that deals with production of RBCs

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15
Q

**Erythropoiesis **increases when?

A

states of **hypoxia **(O2 deficiency)

  • stimulates kidneys to release hormone erythropoietin (EPO)
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16
Q

Erythropoietin (EPO)

A

EPO circulates to red bone marrow

speeds up maturation & release of immature red cells

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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
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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
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19
Q

Reticulocytes

A

immature RBCs

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20
Q

Rate of **Erythropoiesis **

  • measured by?
A

number of immature RBCs (reticulocytes) in peripheral circulation

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21
Q

A low retic count

A

(<.5%) indicates low rate of erythropoiesis

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22
Q

elevated rate

A

(>2%) indicates high rate of erythropoiesis

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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 **
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24
Q

Each RBC contains __ ___ molecules of Hgb

A

280 million

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25
Q

Anemia

A

condition of reduced oxygen carrying capacity of blood due to insufficient RBC’s or hemoglobin (quality/quantity)

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26
Q

Anemia is most often result of? (5)

A
  1. low iron intake
  2. hemolysis
  3. autoimmune disease
  4. blood loss
  5. lack of production in bone marrow
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27
Q

Polycythemia

A

condition of excess number of RBCs

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28
Q

Polycythemia occurs in response to?

A
  1. hypoxia (natural “blood doping” = training at high altitude)
  2. shots of EPO (illegal “doping”)
  3. smoking (Chronic obstructive pulmonary disease- COPD)
  4. dehydration
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29
Q

Types of Anemia (3)

A

1) Iron deficiency anemia
2) Hemorrhagic anemia
3) Sickle-cell disease (SCD) - sickle-cell anemia

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30
Q

1) Iron deficiency anemia

A

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

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31
Q

2) Hemorrhagic anemia

A

result of precipitous blood loss & results in equal decrease in Hct, Hgb content, and RBC count

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32
Q

3) Sickle-cell disease (SCD) - sickle-cell anemia

A

= 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
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33
Q

RBC life cycle

A

only 120 days

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34
Q

To maintain normal numbers of RBCs…

A

new mature cells must enter circulation at rate of at least 2 million/second

    • pace that balances rate of RBC destruction*
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35
Q

Ruptured RBCs - what happens to them?

A

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

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36
Q

Hemolysis

A

rupturing of **erythrocytes **(red blood cells)

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37
Q

WBCs

A

leukocytes

have nuclei & full complement of other organelles

  • but they do not Hemoglobin
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38
Q

Function of WBCs

A

attack pathogens invading body

lymphocytes attack viruses

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39
Q

For diagnostic purposes, physicians measure ..

A

the total number of circulating WBCs

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40
Q

Leukocytosis

A

increased WBC count
10,000/µL

  • usually indicate an infection, surgery or strenuous exercise
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41
Q

Leukopenia

A

decreased WBC count **(< 5,000/µL) **

•usually indicates a severe disease (AIDS, bone marrow failure, severe malnutrition, or chemotherapy)

42
Q

WBC differential

A

test that determines % of each of the **5 types of WBCs **

  • to enhance diagnostic value of WBC count

-

43
Q

Shifts in the normal percentages of circulating WBCs will often point towards? (2)

A

bacterial infection (elevated % of neutrophils)

or

a viral infection (elevated % of lymphocytes)

44
Q

Hemostatis

A

sequence of responses that stops bleeding

45
Q

When blood vessels are damaged/ruptured, the hemostatic response must be… (3)

A

quick

localized to region of damage

carefully controlled in order to be effective

46
Q

(3) mechanisms reduce blood loss

A

1) vascular spasm

2) formation of platelet plug
3) blood clotting (coagulation)

47
Q

1) Vascular spasm

A

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
Q

Vascular spasm

**caused by? (3) **

A

damage to smooth muscle

by substances released from activated platelets

by reflexes initiated by pain receptors.

49
Q

2) Platelet plug
- (3) steps

A

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
Q

platelet derived growth factor (PDGF)

A

hormone that can cause proliferation of vascular endothelial cells, vascular smooth muscle fibers & fibroblasts to help repair damaged blood vessel walls

51
Q

1) platelet adhesion

A

platelets contact & stick to parts of damaged blood vessel (collagen fibers of CT underlying damaged endothelial cells)

52
Q

2) platelet release rxn

A

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
Q

3) platelet aggregation

A

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
Q

Clotting (coagulation)

A

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
Q

Clotting (coagulation) is possible because of?

occurs in?

A

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
Q

(3) stages of clotting

A

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
Q

(2) pathways to activate **clotting **

A

Intrinsic

Extrinsic

  • lead to formation of **prothrombinase **
58
Q

Extrinsic Pathway

A

**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 **
59
Q

**Intrinsic **Pathway

A

<!--StartFragment-->

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 **

<!--EndFragment-->

<!--EndFragment-->

60
Q

Extrinsic Pathway
- speed, steps (general)

A

few steps
occurs rapidly
within seconds once protein Tissue Factor (TF) leaks into blood

61
Q

Intrinsic Pathway
- steps, speed (general)

A

more complex
occurs more slowly
in response to damage to **endothelial cells **or **phospholipids **released by **activated platelets **

62
Q

Common Pathway

A

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
Q

Both extrinsic and intrinsic clotting pathways converge at … where?

A

a common point (pathway) where factor X becomes activated (Xa)

64
Q

Common Pathway - detailed

A

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
Q

Thrombin has **(2) positive feedback effects. **

A

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
Q

Clot Retraction

A

consolidation of the fibrin clot

67
Q

Clot Retraction - process

A

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
Q

Normal retraction depends on?

A

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
Q

Because blood clotting involves amplification & positive feedback cycles, a clot has a tendency to? creating the potential for?

A

enlarge
impairment of blood flow through undamaged vessels

70
Q

**fibrinolytic system **

A

dissolves small, inappropriate clots

  • also dissolves clots at a site of damage once damage is repaired
71
Q
  • *FIbrinolysis**
  • process
A

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
Q

Thrombosis

A

clotting in unbroken blood vessel (usually vein)

73
Q

thrombus

A

clot

74
Q

Thrombus may be initiated by?

A

roughened endothelial surfaces of a blood vessel resulting from

atherosclerosis, **trauma **or infection →induce adhesion of platelets

75
Q

Embolus

A

when blood clot, air bubble, piece of fat or other debris is transported in blood stream

76
Q

Embolus - dangerous?

A

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

77
Q

Atherosclerosis

A

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
Q

Intravascular clotting

  • also form when?
A

when blood flows too **slowly (stasis) **
allows clotting factors to accumulate locally & initiate coagulation cascade

79
Q

Important factors that inhibit thrombosis

A

undamaged blood vessels with smooth surfaces
good circulation
non-sticky platelets
- administration of anticoagulants & platelet inhibiting drugs (aspirin-like) - can reverse thrombus formed

80
Q

Antigens

A

antibody generator
any substance which provokes an adaptive immune response

81
Q

RBCs & antigens

A

RBCs have proteins on surface which act as **antigens (surface markers) **

82
Q

Antigens within same species

A

not necessarily compatible with those of another

83
Q

most significant of the 100 markers currently known to exist on RBCs

A

A and B antigens

84
Q

basis of ABO blood group system

A

presence/absence of **A & B red cell antigens **

- Rh antigen: another major red cell antigen (85% of popn have)

85
Q

Antibodies & Antigens of blood

A

serum contains anti-ABO antibodies of type **opposite **to ABO antigen on red cell surface

86
Q

Type AB

A
  • *universal recipients **
  • dont have Anti-A or Anti-B antibodies to destroy transfused RBCs
87
Q

Type O

A

universal donors

RBCs have no antigens on cell surface to react with recipients serum

88
Q

Agglutination

A

clumping of RBCs

- antigen–antibody response in which RBCs become cross‐linked to one another

89
Q

•Agglutination with an antisera indicates?

A

presence of that antigen on the RBC

90
Q

vIn a blood transfusion, if the recipient receives the wrong blood type.. what happens?

A

** antigen-antibody reactions** will cause a rapid destruction (hemolysis) of donor red blood cells

91
Q

•Giving the wrong type blood can cause… (3)

A

the patient to develop a fever, serious renal failure, or go into shock.

92
Q

Normally blood plasma contains or doesnt contain anti-Rh antibodies?

A

does NOT

93
Q

Rh+

A

RBCs have Rh antigen

94
Q

Rh-

A

lack Rh antigen

95
Q

Rh incompatibility - mother & child

A

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
Q

**Hemolytic disease of the newborn (HDN) **results when?

A

when an Rh+ fetus develops in the womb of Rh- women

97
Q

To prevent HDN

A

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
Q

Intravascular Clotting

A

blood clots form within cardiovascular system

initiated by roughened endothelial surfaces of blood vessels

99
Q

Intravascular Clotting

Blood clots initiated by roughened endothelial surfaces of blood vessels resulting from? (3)

A

atherosclerosis

trauma

infection

100
Q
A

KIN 267 (12 decks)

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