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Physiology > Exam 3: Ch 13 Blood Cardiac Cycle > Flashcards

Exam 3: Ch 13 Blood Cardiac Cycle Flashcards

1
Q

Plasma Protein

A

Constitute 7-9% of plasma

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2
Q

Three types of plasma proteins

A
  • albumins
  • globulins
  • fibrinogen
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3
Q

Albumin accounts for

A
  • 60-80% of PP and smallest;

- made by liver

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4
Q

Albumin Creates

A

colloid osmotic pressure that draws H20 from interstitial fluid into capillaries to maintain blood volume & pressure

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5
Q

Globulins: 3 types

A
  • alpha
  • beta and
  • gamma globulin
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6
Q

Alpha and Beta globulins

A

made by liver and transport lipids and fat soluble vitamins

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7
Q

Gamma globulins

A

antibodies produced by lymphocytes

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8
Q

Fibrinogen

A
  • (4% of PP);
  • produced by liver;
  • serves as clotting factor;
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9
Q

Fibrinogen Converted to

A
  • insoluble threads called fibrin during clotting process
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10
Q

Anemia

A

any condition in which there is an abnormally low [hemoglobin] or RBC count

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11
Q

Iron-deficiency Anemia

A

caused by deficiency of iron

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12
Q

Pernicious Anemia

A

caused by inadequate [vitamin B12], which is needed for RBC production

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13
Q

Aplastic Anemia

A

due to destruction of bone marrow

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14
Q

Polycythemia

A

abnormal increase in RBC

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15
Q

Antigens present on RBC surface specify

A

blood type

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16
Q

Major antigen group is

A

ABO system

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17
Q

Type A blood

A
  • has only A antigens

- People with Type A blood make antibodies to Type B RBCs, but not to Type A

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18
Q

Type B

A
  • has only B antigens

- Type B blood has antibodies to Type A RBCs but not to Type B

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19
Q

Type AB

A
  • has both A & B antigens
  • Type AB blood does not have antibodies to A or B
  • Type AB is “universal recipient”
    because does not make anti-A or anti-B antibodies; Won’t agglutinate donor’s RBCs
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20
Q

Type O

A

has neither A or B antigens
- Type O has antibodies to both Type A and B
- Type O is “universal donor”
because lacks A and B antigens; recipient’s antibodies will not agglutinate donor’s Type O RBCs

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21
Q

If different blood types are mixed

A

antibodies will cause mixture to agglutinate

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22
Q

If blood types do not match

A

recipient’s antibodies agglutinate donor’s RBCs

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23
Q

Rh Factor

A

Is another type of antigen found on RBCs

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24
Q

Rh+ has

A

Rho(D) antigens; Rh- does not

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25
Q

Rh Factor Can cause problems when

A
  • when Rh- mother has Rh+ babies
    • At birth, mother may be exposed to Rh+ blood of fetus
    • In later pregnancies mom may produce antibodies against Rh
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26
Q

Erythroblastosis fetalis

A
  • mom may produce antibodies against Rh

- antibodies cross placenta causing hemolysis of fetal RBCs

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27
Q

Hemostasis

A

cessation of bleeding

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28
Q

Hemostasis Promoted by

A

by reactions initiated by vessel injury

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29
Q

breakage of endothelial lining of vessels exposes

A

collagen proteins in subendothelial C.T. to the blood

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30
Q

breakage of endothelial lining of vessels Initiates

A

3 separate but overlapping hemostatic mechanisms

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31
Q

3 separate but overlapping hemostatic mechanisms

A
  1. Vasoconstriction restricts blood flow to area
  2. Formation of platelet plug
  3. Production of web of fibrin proteins that penetrates and surrounds platelet plug, forming clot
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32
Q

Platelets

A
  • smallest of formed elements
  • lack nucleus
  • are fragments of megakaryocytes
  • amoeboid action
  • constitute most of mass of blood clots
  • last 5-9 days
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33
Q

Intact endothelium physically separates

A

blood from collagen and other clot forming factors

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34
Q

Endothelial cells secrete

A

prostacyclin (PGI2–a prostaglandin) and NO; that inhibit platelet aggregation and are vasodilators

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35
Q

Endothelial cell membranes have

A

enzyme = CD39 whose active site faces blood and converts ADP into AMP and Pi

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36
Q

Endothelial cell membranes inhibits platelet aggregation b/c

A

ADP is released by activated platelets and promotes platelet aggregation

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37
Q

Injured blood vessels =

A

= damage to endothelium;

- allows platelets to bind to exposed collagen

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38
Q

von Willebrand factor

A

increases bond between collagen and platelets by binding to both

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39
Q

Platelets stick to

A

collagen randelease ADP and thromboxane A2 which recruit more platelets and = platelet release reaction occurs

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40
Q

= platelet release reaction occurs

A

= creates platelet plug in damaged vessel

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41
Q

Serotonin & thromboxane A2 stimulate

A

vasoconstriction, reducing blood flow to wound

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42
Q

ADP & thromboxane A2 cause

A

cause other platelets to become sticky & attach & undergo platelet release reaction; this continues until platelet plug is formed

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43
Q

Activation of platelets also causes

A

conversion of soluble PP fibrinogen into insoluble protein = fibrin

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44
Q

Platelets have fibrin binding sites so

A

so platelet plug becomes infiltrated by meshwork of fibrin; clot now contains platelets, fibrin & trapped RBCs

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45
Q

Platelet plug undergoes

A
  • plug contraction to form more compact plug:

- fluid is squeezed from clot

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46
Q
  • Note: serum =
A

plasma w/o fibrinogen

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47
Q

Anticoagulants

Clotting can be prevented by

A
  • Ca+2 chelators (e.g. sodium citrate or EDTA)
  • Heparin
  • Coumarin
48
Q

Heparin

A
  • which activates antithrombin III
49
Q

antithrombin III

A

blocks thrombin, which directly converts fibrinogen into fibrin

50
Q

Coumarin

A

blocks clotting by inhibiting activation of Vit K

51
Q

Vit K works indirectly by

A

reducing Ca+2 availability

52
Q

Cardiac cycle =

A

repeating pattern of contraction & relaxation of heart

53
Q

Systole

A

refers to contraction phase (~0.3 second)

54
Q

Diastole

A
  • refers to relaxation phase (~0.5 second)
  • Both atria contract simultaneously
  • Both ventricles follow 0.1-0.2 sec later
55
Q

End-systolic volume

A

amount of blood left in ventricles at end of systole

56
Q

Stroke volume

A

is amount of blood ejected from ventricles during systole

57
Q

End-diastolic volume

A

is amount of blood left in ventricles at end of diastole

58
Q

As ventricles begin contraction

A

pressure rises closing AV valves = called isovolumetric contraction because all valves are closed

59
Q

When pressure in ventricles exceeds that in aorta,

A

semilunar valves open & ejection begins and as pressure in ventricle falls below that in aorta, back pressure closes semilunar valves

60
Q

When pressure in ventricles falls below atria

A

AVs open & ventricles fill

61
Q

During ventricular diastole

A

ventricles fill ~ 80%

62
Q

Atrial systole sends

A

~ 20 % of the total ventricular blood into ventricles

63
Q

Closing of AV & semilunar valves produces sounds that can be heard thru stethoscope

A
  • lub

- dub

64
Q

Lub

A

(1st sound) produced by closing of AV valves (between atria & ventricles)

65
Q

Dub

A

(2nd sound) produced by closing of semilunars (between ventricles and aorta or pulmonary artery)

66
Q

Heart Murmurs

A

Are abnormal sounds produced by abnormal patterns of blood flow in heart

67
Q

Heart Murmurs

Many caused by

A
  • by defective heart valves
    • can be of congenital origin
    • rheumatic fever
68
Q

in rheumatic fever,

A

damage can be from antibodies made in response to strep infection

69
Q

In mitral stenosis

A

mitral (left A-V) valve becomes thickened and calcified

impairing blood flow from left atrium to left ventricle

70
Q

in mitral stenosis

causes

A

accumulation of blood in left ventricle that can lead to pulmonary hypertension

71
Q

Valves are incompetent when

A

when do not close properly

- can be from damage to papillary muscles

72
Q

Mumurs caused by septal defects are

A
  • septal defects are usually congenital
    due to holes in septum between left and right sides of heart
  • pressure causes blood to pass from left to right
73
Q

Myocardial cells are

A

short, branched, & interconnected by gap junctions

74
Q

myocardium

A

Entire muscle that forms chambers

75
Q

myocardium Works in

A

functional syncitium

because APs originating in any cell are transmitted to all others

76
Q

myocardium Chambers separated by

A

nonconductive tissue

77
Q

In normal heart, SA node in

A

in R-atrium, near superior vena cava functions as pacemaker

78
Q

pacemaker potential

A

Exhibits slow spontaneous depolarization to threshold

79
Q

Membrane voltage begins at

A

at -50mV and gradually depolarizes to -40 threshold

80
Q

Spontaneous depolarization is caused by

A

Na+ flowing through channel that opens when hyperpolarized (HCN (hyperpolarization cyclic nucleotide) channel)

81
Q

At threshold V-gated Ca2+ channels

A
  • open, creating upstroke & contraction

- Repolarization is via opening of V-gated K+ channels

82
Q

Ectopic Pacemakers

A
  • Other tissues in heart are spontaneously active but are slower than SA node
    • are stimulated to produce APs by SA node before spontaneously depolarize to threshold
    • If APs from SA node are prevented from reaching these, they will generate pacemaker potentials
83
Q

Myocardial APs

- Myocardial cells have RMP of

A
  • –90 mV; depolarized to threshold by APs originating in SA node
  • Upstroke occurs as V-gated Na+ channels open
84
Q

Myocardial APs

- MP rapidly increases to

A

+15mV & stays there for 200-300 msec (plateau phase); Plateau results from balance between slow Ca2+ influx & K+ efflux
Repolarization due to opening of extra K+ channels

85
Q

APs from SA node spread through

A
  • atrial myocardium via gap junctions

- But need special pathway to ventricles because of non-conducting fibrous tissue

86
Q

special pathway to ventricles

A

AV node at base of right atrium & bundle of His conduct APs to ventricles

87
Q

In septum of ventricles

A
  • bundle of His divides into right and left bundle branches

- Which give rise to Purkinje fibers in walls of ventricles; these stimulate contraction of ventricles

88
Q

Conduction of APs

A
  • APs from SA node spread at rate of 0.8 -1 m/sec
  • Time delay occurs as APs pass through AV node; has slow conduction of 0.03– 0.05 m/sec
  • AP speed increases in Purkinje fibers to 5 m/sec and ventricular contraction begins 0.1–0.2 sec after contraction of atria
89
Q

Excitation-Contraction Coupling

- Depolarization of myocardial cells opens V-gated Ca2+ channels in sarcolema

A
  • This depolarization opens V-gated and Ca2+ release channels in SR (calcium-stimulated-calcium-release)
    • Ca2+ binds to troponin and stimulates contraction (as in skeletal muscle); During repolarization Ca2+ pumped out of sarcoplasm and into SR
90
Q

Refractory Periods

A
  • Heart contracts as syncytium and thus cannot sustain force; its AP lasts about 250 msec
  • Has a refractory period almost as long as AP
  • Cannot be stimulated to contract again until has relaxed; thus there is no summation
91
Q

Electrocardiogram (ECG/EKG)

A
  • Is a recording of electrical activity of heart conducted thru ions in body to surface and recorded by electrodes placed on the skin
92
Q

NOTE: ECG is not recording of AP!! It is a

A

recording of the electrical activity of the heart

93
Q

Changing position of ECG recording electrodes (leads)

A

a more complete picture

94
Q

3 distinct waves are produced during cardiac cycle

A
  • P wave caused by atrial depolarization
  • QRS complex caused by ventricular depolarization
  • T wave results from ventricular repolarization
  • Atrial repolarization is hidden by the QRS complex
95
Q

Correlation of ECG with Heart Sounds

A
  • 1st heart sound (lub) comes immediately after QRS wave as AV valves close
  • 2nd heart sound (dub) comes as T wave begins and semilunar valves close.
96
Q

Is most common form of arteriosclerosis

A
  • (hardening of arteries);

- Accounts for 50% of deaths in US, Europe, and Japan

97
Q

localized plaques

A
  • (atheromas) reduce flow in an artery

- and act as sites for thrombus (blood clots)

98
Q

Plaques begin at

A

sites of damage to endothelium; from hypertension, smoking, high cholesterol, or diabetes

99
Q

High blood cholesterol is associated with

A
  • risk of atherosclerosis

Cholesterol, is carried in blood attached to LDLs (low-density lipoproteins) and HDLs (high-density lipoproteins)

100
Q

LDLs & HDLs are produced in

A
  • in liver and taken into cells by receptor-mediated endocytosis
    • in cells LDL is oxidized
101
Q

Oxidized LDL

A

can injure endothelial cells facilitating plaque formation

102
Q

Arteries have receptors for

A

for LDL but not HDL (only liver has HDL receptors), which is why HDL is not atherosclerotic

103
Q

Ischemia

A
  • occurs when blood supply to tissue is deficient

- causes increased lactic acid from anaerobic metabolism

104
Q

Myocardial ischemia is most commonly due to

A

atherosclerosis in coronary arteries and is often accompanied by angina pectoris (substernal pain) or left shoulder and arm pain

105
Q

Myocardial infarction (MI)

A

= heart attack
- caused by prolonged (minutes) periods of ischemia resulting in necrosis
= leading cause of death in the world!!

106
Q 
Myocardial infarction (MI) 
Diagnosed by
A

by high levels of creatine phosphate (CPK) & lactate dehydrogenase (LDH), and ↑plasma [troponin]

107
Q

Arrhythmias are

A
  • are abnormal heart rhythms are detectable by changes in ECG
  • Heart rate <60/min is bradycardia;
  • > 100/min is tachycardia
108
Q

Flutter

A

= coordinated contraction rates can be 200-300/min

109
Q

Fibrillation

A

contraction of myocardial cells is uncoordinated & pumping ineffective

110
Q

Ventricular fibrillation

A

is life-threatening

111
Q

Electrical defibrillation

A

resynchronizes heart by depolarizing all cells at same time

112
Q

AV node block occurs

A

when node is damaged

113
Q

First–degree AV node block

A

is when conduction through AV node > 0.2 sec

Causes long P-R interval

114
Q

Second-degree AV node block

A

is when only 1 out of 2-4 atrial APs can pass to ventricles

Causes P waves with no QRS

115
Q

In third-degree or complete AV node block

A
  • no atrial activity passes to ventricles

Ventricles driven slowly by bundle of His or Purkinjes

Physiology (27 decks)

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