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Physiology III > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

What is the #1 cause of death

A

CVD aka Cardiovascular disease

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2
Q

What is the major underlying cause of CVD

A

Ischemia due to atherosclerosis

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3
Q

What is atherosclerosis

A

Plaquing

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4
Q

What is linked to high blood cholesterol

A

Atherogenesis

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5
Q

Leukocyte recruitment and expression of pro-inflammatory cytokines characterize what

A

Early atherogenesis

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6
Q

What promotes thrombosis

A

Inflammatory pathways

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7
Q

What is Thrombosis is responsible for

A

MI and most strokes

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8
Q

What can the nervous system modulate

A

Inflammation

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9
Q

What is Hemostasis

A

Prevention of blood loss

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10
Q

What are the Mechanisms of Hemostasis

A

Vascular Spasm, Form platelet plug, blood coagulation, and fibrous tissue growth to seal

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11
Q

What is vascular constriction associated with

A

Trauma

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12
Q

How do neural reflexes work in Hemostasis

A

SNS induced constriction from pain

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13
Q

What is responsible for most of the constriction in hemostasis

A

Local myogenic spasm

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14
Q

What is especially important in smaller vessels, and includes thromboxane A2 from platelets

A

Local Humoral factors

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15
Q

What is the degree of spasm related to

A

Severity of the trauma

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16
Q

What function as whole cells, but cannot divide

A

Platelets

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17
Q

What do platelets contain

A

Contractile proteins, enzymes, calcium, ADP and ATP, Thromboxane A2, serotonin, growth factors

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18
Q

What is the platelet cell membrane made of that makes it special

A

Glycoproteins that avoid the normal endothelium, but adhere to damaged area

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19
Q

What do the phospholipids of a platelet cell membrane contain

A

Platelet factor 3

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20
Q

What initiates clotting

A

Thromboplastin

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21
Q

When platelets contact a damaged area they:
Select all that apply:
1) Swell
2) irregular form w/ irradiating processes protruding from surface
3) contractile proteins contract causing granule release
4) Secrete ADP, Thromboxane A2 & Serotonin

A

1,2,3,4

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22
Q

What is a Vasoconstrictor and Potentiates the release of granule contents

A

Thromboxane A2

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23
Q

What are these characteristics of 150,000-300,000; important in minute ruptures; half-life of 8-12 days

A

Platelets

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24
Q

What prevents platelet aggregation, produces PGI2 (prostacyclin) and Factor VIII

A

Endothelium

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25
Q

What is factor VIII responsible for

A

Clotting

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26
Q

What is a Vasodilator, Stim platelet adenyl cyclase supressing the release of granules, and limits platelet extension

A

PGI2 (Prostacyclin)

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27
Q

What do Aspirin and Ibuprofen block

A

Fatty Acid Cyclooxygenase

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28
Q

What 2 things do Aspirin and Ibuprofen block production of by blocking fatty acid cyclooxygenase

A

Thromboxane A2 and Prostacyclin

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29
Q

What does FA cyclooxygenase convert ARA to

A

PGG2 and PGH2

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30
Q

What do anticoagulants do

A

Prevent clots from forming

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31
Q

What are the 3 types of anticoagulants

A

Chelators, Heparin, and Dicumarol

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32
Q

Which anticoagulant has complexes with Antithrobin III

A

Heparin

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33
Q

Which anticoagulant tye up calcium (citrate, oxylate)

A

Chelators

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34
Q

Which anticoagulant involves inhibition of Vit. K dependent factors

A

Dicumarol

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35
Q

What synthesizes factors II, VII, IX, X

A

Hepatocytes

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36
Q

Cumadin and Warfarin are what kind of anticoagulant

A

Dicumarol

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37
Q

What is the Lysis of clots used for

A

Dissolves colts that have already formed

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38
Q

What is required for the lysis of clots

A

Plasmin (from plasminogen)

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39
Q

What is plasminogen

A

Inactive form of plasmin

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40
Q

Where are endogenous activators of plasminogen found

A

Tissues, plasma, urine

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41
Q

What are Exogenous activators of plasminogen

A

Steptokinase and tPA (tissue plasminogen activator) 3 hour window for MI and stroke

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42
Q

When does most damage with reperfusion injury occur

A

Upon reperfusion

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43
Q

What specifically does the damage with reperfusion injuries

A

Formation of highly ROS w/ unpaired e- (free radicals)

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44
Q

What is the ability to open up alternate routes of blood flow to compensate for a blocked vessel

A

Collateralization

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45
Q

What may the SNS do in collateralization

A

Impede via vasoconstriction, or augment via release of neuropeptide Y (NPY)

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46
Q

What is a Thrombosis

A

Blood coagulation

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47
Q

What is the extrinsic mechanism of Thrombosis formation

A

Chemical factors released by damaged tissues

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48
Q

What is the intrinsic mechanism of Thrombosis formation

A

Requires only components in blood and trauma to blood or exposure to collagen

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49
Q

What 5 Clotting factors are synthesized in the liver

A

I, II, VII, IX, and X

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50
Q

How does Coumarin (warfarin or cumadin) depress liver formation of II, VII, IX, X

A

Blocking action of Vit. K

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51
Q 
Name the Condition:
Sex linked on X chromosome
almost exclusively males
85% defect in factor VIII
15% defect in factor IX
Can range severe-mild
A

Hemophilia

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52
Q

What is the key step in clotting

A

Conversion of fibrinogen to fibrin which requires thrombin

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53
Q

What is an autoimmune disorder where the body makes antibodies against phospholipids in cell membranes causing abnormal clots to form

A

Antiphospholipid antibody syndrome

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54
Q

Increasing age, Male gender, Heredity (including race), Tobacco Smoke, High blood cholesterol, High blood pressure, Physical inactivity, Obesity/overweight, Diabetes Mellitus, High blood, homocysteine, are all Risk factors for what

A

Heart Disease

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55
Q

What AA in the blood may irritate blood vessels, promoting atherosclerosis

A

Homocysteine

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56
Q

What can cause cholesterol to become oxidized LDL

A

Homocysteine

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57
Q

T/F: Homocysteine is more likely to make blood clot

A

True

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58
Q

What can high levels of Homocysteine be reduced by

A

Increased intake of Folic Acid, B6 and B12

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59
Q

What antigen sets on RBCs are most likely to cause transfusion rxns if they are mismatched

A

A, B, O and the Rh factor

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60
Q

What are A and B antigens on RBCs known as

A

Agglutinogens

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61
Q

Why are A and B antigens known as Agglutinogens

A

When they are on RBCs, they cause most blood transfusion rxns

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62
Q

What is significant about the O antigen on a RBC

A

It is essentially functionless

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63
Q

Genetic locus has three alleles, IA, IB, IO that can combine into how many combinations

A

6

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64
Q

What determines if a person has one, none, or both surface antigens

A

Inheritance

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65
Q

When are Agglutinins produced

A

They arise spontaneously after birth (2-8 months)

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66
Q

What are Agglutinins

A

Soluble antibodies on RBCs

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67
Q

When are Agglutinins not produced

A

When the corresponding Agglutinogens are present on the RBC

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68
Q

When do antibodies peak, then decline for the rest of a persons life

A

Age 10

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69
Q

How common iss immediate hemolysis occur in mismatched transfusion

A

Uncommon/Less common

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70
Q

How common is delayed hemolysis in mismatched transfusions

A

Common/More common

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71
Q

Which antibody is primarily responsible for the lysis of RBCs

A

IgM

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72
Q

What is the most lethal effect of a mismatched transfusion reaction

A

Kidney failure

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73
Q

What blood type is the universal donor

A

O

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74
Q

What is the universal recipient

A

AB

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75
Q

Why does kidney failure occur in mismatched transfusion rxns

A

Toxic substances are released from the hemolysed RBCs

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76
Q

What potentially deadly effect can kidney failure lead to

A

Circulatory shock

77
Q

What from lysed RBCs can precipitate and block renal tubules

A

Hemoglobin

78
Q

T/F: Spontaneous Agglutinins can arise just like the A-B-O system

A

FALSE, Unlike the A-B-O system, Spontaneous Agglutinins CANNOT arise

79
Q

What are the 6 Rh antigens (Rh factor)

A

C, D, E, c, d, e

80
Q

What antigen is the most common and antigenic (85% of US pop)

A

D antigen (Rh +)

81
Q

What is the Rh factor when the D antigen is missing

A

Rh-

82
Q

What occurs when Rh+ blood is given to an individual with Rh- blood

A

Antibodies are created and slowly build until they reach max concentrations 2-4 months later

83
Q

What is aka “Hemolytic disease of the Newborn”

A

Erythroblastosis Fetalis

84
Q

Agglutination of fetal blood releases Hgb, which is converted by macrophages into bilirubin which causes

A

Jaundice

85
Q

In most cases of Erythroblastosis Fetalis, the mother is RH(___) and the father is Rh(___), with the fetus being Rh(___) received from the father

A

Mom Rh-
Dad Rh+
Fetus Rh+

86
Q

T/F: Erythroblastosis Fetalis is typically not seen in the firstborn, but more in the 2nd, and more again in the 3rd

A

TRUE

87
Q

What can happen after birth in a newborn that had Erythroblastosis Fetalis

A

Mother’s Rh Agglutinins can still circulate for 1-2 moths and destroy fetus RBCs leading to anemia

88
Q

Erythroblastosis Fetalis can result in the enlargement of what in neonates

A

Liver and Spine

89
Q

Bilirubin may precipitate in neurons of the brain causing what

A

Mental impairment (kernicterus)

90
Q

What is the Tx for erythroblastosis Fetalis

A

Replacement of Neonate’s blood with Rh- blood

91
Q

What can be used to prevent Erythroblastosis Fetalis

A

Rh immunoglobulin globulin (RhoGAM), and anti-D antibody, given at 28-30 weeks of gestation

92
Q

What is different about heart m.

A

It is Specialized excitatory and conductive fibers (AS node, AV node, Purkinje fibers

93
Q

What allows for the functional syncytium of the heart

A

The presence of intercalated discs

94
Q

What are intercalated discs

A

Low resistance pathways connecting cardiac cells end to end with the presence of gap junctions

95
Q

What is the duration of the AP in cardiac m.

A

.2-.3 sec

96
Q

What are the types of channels in cardiac m.

A

Fast Na+, Slow Ca++/Na+, and K+

97
Q

When do we see a sharp inc. in Na+ permeability

A

Onset of depolarization

98
Q

When do we see an inc. in Ca++ permeability

A

During the plateau

99
Q

When do we see an inc. in K+ permeability

A

During the resting polarized state

100
Q

What does Tetradotoxin do to Na+ channels

A

Tetradotoxin blocks them selectively changing a fast response to a slow response

101
Q

If ion channels are open, what will the ion seek

A

The nearest equilibrium potential

102
Q

What does membrane permeability depend on

A

Ion channels (open or closed)

103
Q

What is concentration gradient favoring ion movement in one direction offset by

A

Electrical gradient

104
Q

What is Er

A

Resting membrane potential

105
Q

During Er in cardiac m., what are the states of the channels (open/closed)

A

Fast Na+ and slow Ca++/Na+ are closed and K+ are open

106
Q

What is the net charge change accomplished by the Na+/K+ pump

A

Net loss of one + charge from int. Of cell keeping the interior of cell negative

107
Q

What can bind to and inhibit the Na+/K+ pump

A

Digitalis

108
Q

What is an absolute refractory period, and when does it occurs

A

Inability to re-stim cardiac death cell, and occurs during the plateau

109
Q

What is the relative refractory period, and when does it occur

A

It requires a supra-normal stimulus during repolarization

110
Q

What is different about the refractory periods in a slow response cardiac m. Cell

A

Relative refractory period is prolonged and refractory period is ~25% longer

111
Q

Why are refractory periods prolonged in slow cardiac m. Cells

A

AV node and bundle, serves to protect ventricles from supra-ventricular arrhythmias

112
Q

What is the normal pacemaker of the heart

A

SA node

113
Q

What structure has a self excitatory nature, Less neg. Er, Spontaneously depolarizes at fastest rate, and contracts feebly

A

SA node

114
Q

If you drive a self-excitatory cell at a rate faster than its own inherent rate, what will happen

A

The cell’s own automaticity will be suppressed

115
Q

What is the job of the AV node

A

Delay the wave of depolarization from entering the ventricle

116
Q

What does the AV node allow the atria to do

A

Contract slightly ahead of the ventricles (.1 sec delay)

117
Q

What is the conduction velocity like in the AV node

A

Slow due to smaller diameter fibers

118
Q

What can the AV node do in absence of the SA node

A

May act as the pacemaker, but at a slower rate

119
Q

What happens to the Cycle length as HR Increases

A

CL decreases

120
Q

Which is shorter at a resting HR, systole or diastole

A

Systole

121
Q

At a high HR, what may not fill adequately

A

The ventricle

122
Q

During systole perfusion of the myocardium, what may restrict reperfusion

A

Contracting Cardiac m. Compressing blood vessels (esp. LV)

123
Q

Isovolumic Contraction and ejection describe what part of the cardiac cycle

A

Systole

124
Q

What phase of the cardiac cycle involves, isovolumic relaxation, rapid inflow, diastasis, and atrial systole

A

Diastole

125
Q

What is End Diastolic Volume (EDV)

A

Volume in ventricles at the end of filling

126
Q

What is End Systolic Volume (ESV)`

A

Volume in ventricles at the end of ejection

127
Q

What is stroke volume

A

EDV-ESV; volume ejected by ventricles

128
Q

What is Ejection fraction

A

% of EDV ejected, normal is 50-60%

129
Q

What is the stretch on the wall prior to contraction

A

Preload (proportional to the EDV)

130
Q

What is the impedance that the heart has to pump against Asa blood is ejected

A

After load

131
Q

What is the A wave associated with

A

Atrial Contraction

132
Q

What is the C wave associated with

A

Ventricular contraction

133
Q

What is the V wave associated with

A

Atrial filling

134
Q

What do valves open with

A

A forward pressure gradient

135
Q

What do valves close with

A

A backward pressure gradient

136
Q

What are the AV valves of the heart

A

Mitral and Tricuspid

137
Q

What are the Semilunar valves of the heart

A

Aortic and Pulmonic

138
Q

What valves have a stronger construction

A

Semilunar (Aortic and Pulmonic)

139
Q

What valves are thin and flimsy, have chorda tendinea, and papillary m.

A

AV valves (Mitral and Tricuspid)

140
Q

What is the function of Chorda Tendineae

A

Prevent valve prolapse

141
Q

What is the function of papillary muscles

A

Inc. tension on Chorda Tendineae

142
Q

What is a stenotic valve

A

Valve not open fully

143
Q

What is a valve that does not close fully

A

Insufficient/regurgitant/leaky

144
Q

What is vibrational noise called with valvular dysfunction

A

A murmur

145
Q

When are aortic/pulmonary stenosis and mitral/tricuspid insufficiency heard

A

Systolic

146
Q

When are aortic/pulmonary insufficiency and mitral/tricuspid stenosis heard

A

Diastolic

147
Q

What can be heard in both systolic and diastolic

A

Patent ductus arteriosis or combined valvular defect

148
Q

What is the Law of Laplace

A

At a given operating pressure, as ventricular radius inc., developed wall tension inc.

149
Q

What is anything that affects HR called (inc. or dec.)

A

Chronotropic

150
Q

What is anything that affects conduction velocity

A

Dromotropic

151
Q

What is anything that affects the strength of contraction called

A

Inotropic

152
Q

What is the Frank-Starling Law of the Heart

A

W/in physiologic limits, the heart will pump all the blood that returns to it without allowing excessive damming of blood in veins

153
Q

What does inc. venous return cause

A

Inc. stretch of cardiac m. Fibers

154
Q

What are the intrinsic effects of Frank-Starling

A

Inc. cross-bridge formation, inc. Ca++ influx, and inc. stretch on SA node

155
Q

What is Heterometric auto regulation

A

Within limits, as cardiac fibers are stretched, the force of contraction is increased

156
Q

What is Homeometric auto regulation

A

Ability to inc. strength of contraction independent of a length change

157
Q

What 3 factors can induce Homeometric autoregulatoin

A

Flow, Pressure, and Rate

158
Q

What will direct stretch on the SA node cause

A

Inc. Ca++ and/or Na+permeability which will inc. HR

159
Q

The autonomic nervous system, Hormonal, Ionic, and Temperature influences are all what kind of influences

A

Extrinsic

160
Q

What effect does Sympathetic innervation have on the heart

A

+ HR, + strength of contraction, and + conduction velocity

161
Q

What effect does Parasympathetic innervation have on the heart

A
  • HR, - Strength of contraction, and - conduction velocity
162
Q

How does the ANS effect SNS interaction with the heart

A

SNS effects are blocked using propranolol (beta blocker)

163
Q

What effect does the ANS have on parasympathetic nervous system

A

Para effects are blocked using Atropine, blocking muscarinic receptors (inc. HR and strength of contraction dec.

164
Q

What exerts a dominant inhibitory influence on HR

A

Parasympathetic NS

165
Q

What exerts a dominant stimulators influence on strength of contraction

A

Sympathetic NS

166
Q

Direct innervation of Cardiac cells accounts for most of what

A

The SNS effect. Norepinephrine actin on Beta-1 receptors (85%)

167
Q

What causes indirect effects of SNS influence

A

Circulating Catecholamines from adrenal medulla find way to cardiac Beta-1 receptors (15%)

168
Q

Stimulation of the left stellar ganglion does what

A

Dec. ventricular fibrillation threshold, and prolonged QT interval

169
Q

What does stim. Of the right stellar ganglion do

A

Inc. ventricular fibrillation threshold

170
Q

The Cardioaccelerator (Bainbridge) reflex, helps to prevent what

A

Damning of blood in the heart and central veins

171
Q

The Benzold-Jarisch relex relates to what structures

A

Baroreceptors in ventricles

172
Q

What does the Benzold-Jarisch reflex result in

A

Hypotension and Bradycardia

173
Q

What stimulates the Benzold-Jarisch reflex

A

Occlusion of circumflex artery and Inc in LVP and LV volume (aka aortic stenosis0

174
Q

What are the major thyroid hormone influences on the heart

A

+ Inotropic, + Chronotropic, and Inc. in CO by Inc. BMR

175
Q

What ionic effect does elevated K+ have

A

Dilation and flaccidity of cardiac m. And dec. in resting membrane potential

176
Q

What ionic effect can elevated Ca++ have on the heart

A

Spastic Contractions

177
Q

What effect does inc. temp have on HR and strength of contraction

A

HR inc 10 beats beer 1 degree inc. and Temporary inc in strength of contraction

178
Q

What effect does a dec. in temp have on HR and strength of contraction

A

Dec. HR and strength of contraction

179
Q

What is the preferred energy substrate for cardiac m.

A

Fatty acids-70% preferred, can also use glucose, glycerol, lactate, pyruvate, and AAs

180
Q

75% of the energy the heart uses is converted to what

A

Heat

181
Q

The 25% of energy used as work is broken down into what

A

Pressurization of blood (>99%) and Acceleration of blood (

182
Q

Pressurization of the blood is what kind of energy

A

Potential energy

183
Q

What is the acceleration of blood to its its ejection velocity is what kind of energy

A

Kinetic

184
Q

What does an EKG measure

A

Potential differences across the surface of the myocardium with respect to time

185
Q

Give the ranges: Normal HR, Tachycardia, Bradycardia

A

N 60-80, T >100, and B

186
Q

What does the P wave signify

A

Atrial Depolarization

187
Q

What does the QRS complex signify

A

Ventricular Depolarization

188
Q

What does the T wave signify

A

Ventricular Repolarization

189
Q

Why can you not see the atrial Repolarization wave

A

It is buried in the QRS complex

Physiology III (2 decks)

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