BLOCK 2 Flashcards

1
Q

What is the effect of angiotensin II in the kidney?

A

Increases activtiy of Na+/H+ exchanger

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2
Q

effect of beta blockers?

A

Inhibit insulin release

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3
Q

What is the role of ACE enzyme during hypotension?

A

Breaks down bradykinin, a potent vasodilator

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4
Q

Effect of progesterone on respiratory centre?

A

Increases tidal volume and ventilation due to increased CO2 sensitivity

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5
Q

What causes increased cardiac output?

A

Increased stroke volume

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6
Q

What is the physiological response to hypoxia?

A

Vasoconstriciton of pulmonary arteries, increased tidal volume and RR

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7
Q

What is lung compliance?

A

Ability to expand- the greater the elastic recoil, the lower the lung compliance

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8
Q

What is pulmonary oedema?

A

Alvoeli fill with fluid that exert mechanical stress to reduce lung compliance

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9
Q

What is the effect of irritant receptors when activated?

A

Bronchospasm

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10
Q

Where are the inspiratory and expiratoryneurones found?

A

Medulla

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11
Q

What is the ventral group?

A

Neurons in medulla which cause forced voluntary expiration, such as cough. It sends inhibitory impulses to pontine apneustic centre.

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12
Q

What is the pneumotaxic centre?

A

Upper pons area which ihnibits inspiration and fine tunes RR.

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13
Q

What is the apneustic centre?

A

Located in lower pons which stimulates respiration. Inhibited by pneumotaxic centre to reduce respiration.

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14
Q

What do central cehmoreceptors respond to?

A

Located in medulla and respond to increased H+ in brain interstital fluid.

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15
Q

What depresses the respiratory medullary centre?

A

Opiates

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16
Q

Effect of lung stretch receptors?

A

Reduces RR rate

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17
Q

Where does automatic involuntary control of respiration occur?

A

Medulla

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18
Q

What is the role of type 1 pnuemocytes?

A

Gas exchange

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19
Q

Clara/club cells

A

Produce lysosyms and glycosaminoglycans found in the terminal bronchioles. They are columnar/cuboidal with microvilli. They are non ciliated and don’t produced mucous

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20
Q

Pleural pressure

A

Pressure surronding lung in pleural space. It is negative if it is below atmospheric pressure when doing quiet breathing.

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21
Q

What is the function of pulmonary surfactant?

A

Reduces surface tension in alevoli to prevent collapse and reduce effort of breathing

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22
Q

What is metabolic acidosis?

A

Caused by gain of acid such diabetic ketoacidosis due to severe insulin deficiency, Addison’s disease with excess cortisol or diarrhoea with loss of bicarbonates.

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23
Q

What increases lung compliance?

A

Age and emphysema which reduce elastic tissue.

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24
Q

What decreases lung compliance?

A

Pulmonary oedema, pulmonary fibrosis due to increased elastic tissue.

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25
Q

What is respiratory acidosis?

A

Caused by hypoventilation which increases CO2 due to oedema, COPD or sedatives like benzodiazeopine for anxiety or opiate overdose. There is excess H+ excretion and HCO3- retainment to compensate.

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26
Q

What is metabolic alkalosis?

A

Increase in bicarbonate levels due to activation of renin-angiotensin-aldosterone system which causes aldosterone release for reabsoprtion of Na+ for loss of H+ via exchanger. This occurs in Cushing’s syndrome, with diuretics, congenital adrenal hyperplasia which increase BP. Loss of H+ can cause metabolic aklaosis due to vomiting that loses stomach acid.

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27
Q

What is respiratory alkalosis?

A

Hyperventilation causing loss of CO2 due to hypoxia in high altitude or pulmonary embolism, CNS stimulation due to stroke or haemhorrage,

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28
Q

What stimulates central chemoreceptors?

A

Arterial CO2

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29
Q

How does hypercapnia affect the brain?

A

Causes cerebral vasodilation which may increase intracranial ressure

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30
Q

Trachea origin

A

C6 and terminates in T4/T5 for bifurcation

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31
Q

Functional vital capcity- normal

A

Obstructive conditions

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32
Q

Normal FEV1/FVC

A

Restrictive lung disease or normal lungs

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33
Q

Low FEV1/FVC

A

Obstructive lung disease

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34
Q

Functional vital capacity- low

A

Restrictive lung disease

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35
Q

What is an obstructive lung disease?

A

Airflow blockage due to emphysema, chronic bronchitis, asthma, bronchiectasis

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36
Q

What is a restrictive lung disease?

A

Reduced lung elasticity or chest eall expansio n that reduces volume that lungs can hold. Includes pulmonary fibrosis, pulmonary oedema and penumonia. These decrease lung compliance.

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37
Q

Where is rhythm of breathing cotrolled?

A

Medulla

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38
Q

Where does troponin I bind to?

A

Actin to hold troponin-tropomyosin complex in place

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39
Q

How do cardiac myocytes interact?

A

Via gap junctions.

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40
Q

Which muscles do not have a neuromasuclar junction?

A

Cardiac myocytes

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41
Q

Which part of the heart depolarises the fastest?

A

SA

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42
Q

What is normal ejection fraction?

A

55-75%

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43
Q

Location of baroreceptors?

A

Caortid sinus located in the internal carotid artery and aortic arch which detects BP

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44
Q

Starling’s law

A

Higher EDV , higher the stroke volume to a point. Venous return increases stroke volume

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45
Q

What phase in the ECG has slow calcium influx?

A

Phase 2

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46
Q

Effect of inhibiting Na+/K+ ATPase

A

Increases myocradial contractility but reduces arrythmia

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47
Q

Afterload

A

Force to overcome for contraction

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48
Q

What increases afterload?

A

Ventricular dilation which is when the ventricle dilates

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49
Q

Effect of stimulation of baroreceptors

A

Parasympathetic discharge to the SA node to decrease firing

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50
Q

Location of arterial barorceptors

A

Carotid sinus and aortic arch

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51
Q

PR interval

A

Time taken for excitation to spread from SA to the ventricles Delay at the AV node to cause atrial contraction. Then, there is conduction of AV node and AV bundle of His

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52
Q

What is the indication of tall T waves?

A

Hyperkalemia and ischaemic heart disease

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53
Q

What is the indication of T wave inversion?

A

Ischaemic heart disease

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54
Q

Absence of P wave

A

Issue with atrial depolarisation-> atrial fibrillation.

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55
Q

Atrial fibrillation

A

Chaotic signal from SAN which override pace maker cells which causes unsynchronous contraction of ventricles and atria. Associated with mitral valve disease

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56
Q

What is valvular heart disease?

A

Leaks blood back into chambers

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57
Q

What is S1 sound?

A

Lub sound caused by the atrioventricular mitral and tricuspid valves closing

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58
Q

What is the S2 sound?

A

Dub sound caused by the aortic valves closing.

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59
Q

What is stenosis?

A

Stiffening of the aortic valve which causes heart murmur

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60
Q

What is regurgitation?

A

Backflow of blood that causes heart murmur

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61
Q

What does troponin T bind to?

A

Tropomyosin

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62
Q

Cardaic output

A

Heart rate x stroke volume

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63
Q

ST segment

A

Ventricular depoalrisation- indicator for myocardial infarction

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64
Q

How to find stroke volume?

A

EDV- ESV

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65
Q

Action of Atrial natriuretic peptide

A

Antagonist of angiotensin II

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66
Q

B-type natriuretic peptide

A

Suppresses sympathetic tone and inhibits renin-angiotensin II

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67
Q

What is the role of renin

A

Angiotensionogen II to angiotensin I

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68
Q

What is preload?

A

EDV- stretch of ventircles at the end of diastole

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69
Q

Where is the SAN located?

A

Right atrium at the superior crista terminalis

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70
Q

Location of AV node

A

Atrioventricular septum

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71
Q

When does K+ efflux occur?

A

Repolarisation in eCG

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72
Q

Which electrolyte maintains resting potential of ventricualr electrolyte?

A

Potassium

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73
Q

Which part of the eCG is when the entire ventricle is depolarised?

A

ST segment

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74
Q

Sequence of cardiac contraction

A

SA node -> atria -> AV node -> Bundle of His -> right and left bundle branches -> Purkinje fibres

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75
Q

Which part has the highest conduction velocity?

A

Purkinje fibres

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76
Q

Which part of the heart has the slowest conduction velocity?

A

AV node

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77
Q

What is average cardiac output?

A

5L/min

78
Q

What causes plateau of action potenital?

A

Slow influx of calcium

79
Q

What maintains the electrical gradient?

A

Potassium influx in phase 4 due to Na+K+ ATPase along with sodium efflux

80
Q

What contirbutes to most of total peripheral resistance and BP stability?

A

Arterioles

81
Q

What prevents fast atrial rate from spreading to the ventricles?

A

AVN

82
Q

When does atrial repolarisation occur?

A

During QRS complex

83
Q

What affects PR interval?

A

Increases conduction velocity

84
Q

What causes T wave shape?

A

Ventricular repolarisation due to K+ efflux

85
Q

Noradrenaline

A

Binds to B1 receptors in SAN node

86
Q

JVP a wave

A

Atrial contraction- absent in atrial fib

87
Q

What is JVP c wave?

A

Closure of tricuspid valve on the right side of the heart

88
Q

What is the v wave?

A

Passive filling of blood in atria against closed tricuspid valve

89
Q

What is the x descend?

A

Fall in atrial pressure during ventricular systole

90
Q

What is the y descent?

A

Opening of tricuspid valve

91
Q

Which part of JVP occurs in S1?

A

A wave and c wave

92
Q

Which part of JVP occurs in S2?

A

X descent, v wave and y descent

93
Q

What happens after birth?

A

Closure of foramen ovale, ductus arteriosus and umbilical vessels.

94
Q

What is the role of the ductus venosus?

A

IVC and umbilical vein

95
Q

Precursor to aorta

A

Truncus arteriosus

96
Q

Truncus arteriosus

A

Gives rise to the ascending aorta and pulmonary trunk

97
Q

Precursor to SVC

A

Right common cardinal vein

98
Q

Precursor to ligamentum arteriosum

A

It is an anchor of the aortic arch- precursor ids ductus arteriosus

99
Q

Precursor to smooth RA?

A

Sinous venosus- right portion

100
Q

Precursor to coronary sinous

A

Sinous venosus- left portion

101
Q

Progenitor of primitive ventircke

A

Forms majority of left ventirlce- gives rise to trabeculated

102
Q

Precursor to trabeculated ventricles

A

Bulbos cordis- smooth right ventirlce and outflow of left and right

103
Q

What is the precursor for the AV and semilunar valves?

A

Endocardial cushion

104
Q

What is the umbilical ligament give rise to?

A

Urachus remnant

105
Q

Tetrology of the Fallot

A

Ventiricular hypertropy, aortic valve hypertropy, pulmonary stenosis and ventricular septal defect. It causes hypoxia and cyanosis, SOB, heart murmur.

106
Q

What is important for the aorta-pulmonary spiral to form?

A

Migration of neural crest cells

107
Q

Innervation for speech

A

Vagus nerve

108
Q

ansa cervicalis

A

Anterior to the carotid sheath and innervates the strap muscles like strenohyoid, sternothyroid, omohyoid

109
Q

Chordae tendinae

A

Attached to valve. Chordae tendinae are linked to ventricle by papillary muscles

110
Q

T12

A

Aorta, thoracic duct, azygous vein

111
Q

Where does the thesbian veins drain into?

A

Drain myocardium into all heart chambers, not limited to coronary sinus

112
Q

What is located in superior mediastinum?

A

SVC, Brachiocephalic vein, thorat and supper chest

113
Q

Anterior mediastinum

A

Lymph node, fat, thymic remnant

114
Q

Middle mediastinum

A

Pericardium, main bronchi, arch of azygous vein, aortic root

115
Q

Posterior mediastinum

A

Sympathetic nerve trunk, splanchnic nerve, thoracic aorta, oesophagus

116
Q

Where does IVC originate?

A

L5

117
Q

What structure is most anterior to the hila?

A

Phrenic nerve

118
Q

What does right coronary artery supply?

A

AV node, SAN, right atria, most of right ventircle

119
Q

Which artery bifurcates at the parotid glannd?

A

External carotid artery

120
Q

Which lung has two fissures?

A

Right lung

121
Q

What separates the tunica media from the other structures?

A

Internal elastic lamina from the tunica intima and external elasatic lamina from tunica adventitia

122
Q

Tunica intima

A

Innermost layer of endothelila cells separated by gap junctions

123
Q

Progenitor of right common carotid?

A

Right brachiocephlaic artery- gives rise to right subclavian artery and right common carotid

124
Q

Retromandibular vein progenitor

A

Maxillary vein

125
Q

Parathyroid veins

A

Thyroid plexus of veins

126
Q

Effect of leukotrienes

A

Bronchoconstriction and implicated in asthma

127
Q

Effect of prostacyclin

A

Vasodilation

128
Q

Stroke volume

A

Volume of blood pumped out of the heart in one contraction

129
Q

What increases blood pressure?

A

Length (think if someone gains weight)P), reduce diameter, viscosity

130
Q

What is JVP?

A

Pressure of blood in the internal jugular vein and in the right atria which is directly connected without any valves. It is covered by the sternocleoidomastoid mastoid. Cannot be palpated but can be seen on the right side in a 45 degree angle

131
Q

What does JVP over 3cm mean?

A

High pressure due to issues with heart expansion, pressure system

132
Q

How to find flow?

A

It is cross sectional area x velocity.Volume of fluid moving in a given time period.

133
Q

What increases velocity?

A

Reducing cross sectional area and radius.

134
Q

How to find pressure?

A

(Q)Flow x resistance (R)

135
Q

Resistance

A

Change in pressure/flow

136
Q

What does Poisuelle’s law describe?

A

Factors which affect flow

137
Q

Effect of polycythaemia

A

Increases blood viscosity to decrease flow

138
Q

Where is BP highest in the heart?

A

Left aorta

139
Q

Where is BP lowest in the heart?

A

Right atria

140
Q

Where is resistance highest at rest?

A

Body > Organs > Brain > Muscles > Heart

141
Q

How does resistance change during exercise?

A

Muscles and heart increase, organs decrease. Brain stays the same

142
Q

What is the relationship between flow and pressure?

A

Non linear

143
Q

Where is urine collected?

A

Bowman;s capsule of kidney

144
Q

Effect of ANP and BNP

A

Activates cGMP for vasodilation and increase urinary excretion cGMP inhibits aldosterone and renin scretion.

145
Q

How is ANP activated?

A

Releases CORIN protein

146
Q

How is BNP activated?

A

Releases FURIN enzyme

147
Q

Where is renin released?

A

Macula densa located in the DCT- epithelial cells that detect Na+. It is activated by sympathetic activity.

148
Q

Effect of renin?

A

Conversion of angiotesinogen -> angiotensin I

149
Q

Where is ACE released?

A

In the lungs. It acts on angiotensin I in bloodstream to form angiotesin II.

149
Q

Effect of angiotensin II

A

It is a potent vasoconstricter of blood vessels, increases Na+ and Cl- reabsorption in the PCT and causes aldosterone release from adrenal gland. Breaks down bradykinin, a vasodilator.

150
Q

How are cardiac myocytes connected?

A

Intercalacted discs

151
Q

What is dromotropy?

A

Spped of impulse conducntion in AVN

152
Q

Action of cardiac glycosides?

A

Inhibiting Na+/K+ ATPase pump

153
Q

Effect of noradrenaline on SAN

A

Activation of low voltage T-type calcium channels and funny Na+ channels for depolarisation. Depolarisation is automatic

153
Q

How long is cardiac cycle?

A

0.8S

154
Q

Ejection fraction

A

Stroke volume/end diastolic volume. Measure of ventricular performance

155
Q

Atrial reflex

A

Atrial pressure increases heart rate

156
Q

What decreases ESV?

A

Sympathetic stimulation, shorter filling time and less venous return. These reduce EDV and stroke volume

157
Q

What increases stroke volume?

A

Venous return, filling time, sympathetic stimulation that increases EDV

158
Q

Where do veins drain in the heart?

A

Into coronary sinus, located in right atria

159
Q

What vein is located in left atria?

A

Obliquevein

160
Q

Which vein is in the right side down the septum?

A

Middle cardiac vein

161
Q

Wich vein is located behind left atria, between the left and right pulmonary veins?

A

Pericardial sinus that separates arterial and venous flow

162
Q

Epithelia of primary and secondary bronchi?

A

Pseudostratified cilitated columnar eptihelia with C shaped hyalien cartilage in primary brocnhi. Secondary bronchi has plates of hyaline cartilage.

163
Q

Epithelia of tertiary bronchi?

A

Columnar epithelia, smooth muscle,

164
Q

Epithelia of respiratory bronchi?

A

Sacs in the walls of terminal bronchi- ciliated cuboidal epithelia with clara cells and evaginations of primary alveoli

165
Q

Terminal bronchi epithelia?

A

Last part of conducting tract. It has pseudostratified columnar epithelia, cilitated cuboidal epithelia and clara cells only, no goblet cells.

166
Q

What regenerates alveolar penumocytes?

A

Type 2 pneumocytes. Hyperplasia is an indicator for injury

167
Q

What are the stem cells of the respiratory tract?

A

Basal cells

168
Q

What keeps olfactory mucosa moist?

A

Bowman’s gland

169
Q

What covers most of the alveolar surface?

A

Type 1 pneumocytes which are simple squamous with occluding jiunctions. They have flat elongated nuclei.

170
Q

Where is surfactant produced?

A

Type 2 pneuocytes. They have reticular fibres and elastic fibres for alveolar elasticity.

171
Q

Effect of increased pulmonary pressure?

A

Decreased cardiac output

172
Q

Haldane effect

A

Uptake of O2 by deoxyhaemaglobin

173
Q

Bohrn Effect

A

Release of 02 from HbO2 due to increased levels of CO2 in the blood/lower ph

174
Q

Hypxoic drive

A

Body uses oxygen chemoreceptors to regulate respiration

175
Q

What is the first phase of ventircular contraction?

A

Isovolumetric contraction- ventiruclar pressure increases when the asemilunar valves are closed

176
Q

What tis the final stage of the cardiac cycle?

A

Isovolumic ventricular relaxation

177
Q

Which vein is on the septum of the left heart?

A

Great cardiac vein

178
Q

Where are small cardiac veins found commonly?

A

Most are in right atria.

179
Q

Location of vasa vasorum?

A

Tunica intima and tunica media. In the tunica

180
Q

What is the vasa vasorum internae?

A

Directly from main artery branch

181
Q

What is vasa vasorum externae?

A

Branch of main artery

182
Q

What regulates blood flow?

A

Metaarterioles

183
Q

What affects venous return?

A

Sympathetic innervation via vasoconstriction, respiratory pump and skeletal muscle pump

184
Q

What maintians pressure gradient?

A

Elastic conducting arteries

185
Q

Site of thrombogenesis?

A

Tunica intima

186
Q

What happens to muscles during contraction?

A

I band and H zone shortens. A band stays the same.

187
Q

Actin only area

A

I band

188
Q

A band

A

Actin and myosin