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MD3001 > Week 1 > Flashcards

Week 1 Flashcards

1
Q

Describe the Fascia of the neck?

A
  • Neck is composed of columns surrounded by fascia.
  • Create potential spaces between muscles in different columns which allows movement without effecting underlying structures.
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2
Q

What is Prevertebral Fascia?

A
  • Neuro-musulo-skeletal
  • A deep layer of deep cervical fascia surrounds vertebral column and associated muscles.
  • Extends from base of skull to coccyx.
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3
Q

What is Pretracheal fascia?

A
  • Surrounds the visceral compartment of the neck
  • Fascial membrane enclosing the esophagus, trachea and thyroid gland.
  • Along with buccopharyngeal fascia is known as the visceral fascia
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4
Q

What is Buccopharyngeal fascia?

A
  • Posterior part of the pretracheal layer of the deep cervical fascia that separates the pharynx and esophagus.
  • Allows sliding of the Pharynx when we swallow.
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5
Q

What is the Carotid sheath?

A
  • Fascial membrane enclosing the internal jugular vein, vagus nerve and common carotid artery.
  • Carotid neurovascular bundle with carotid sheath on each side.
  • Extends from base of skull to root of neck.
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6
Q

What is investing fascia?

A

Most superficial layer of deep cervical fascia surrounding the entire neck

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7
Q

What are the 3 Potential spaces?

A
  1. Exist between muscles on floor of the mouth.
  2. Retropharyngeal space between prevertebral and pretracheal surrounding anterior column.
  3. Pretracheal space from neck to superior mediastinum.
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8
Q

What is the Retropharyngeal space?

A
  • Potential space between the buccopharyngeal and prevertebra fascia.
  • Potential for infections of face and neck, especially teeth (abcesses).
  • Extends all the way up to base of skull and down to diaphragm.
  • Passes behind left atrium in mediastinum, risk of infection to heart.
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9
Q

What is the Pretracheal space?

A
  • Between investing and pretracheal fascia

- This space is continuous with the anterior mediastinum of the thorax

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10
Q

Sternocleidomastoid separates the neck into what 2 Neck triangles?

A
  1. anterior

2. posterior.

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11
Q

Describe the Posterior triangle?

A
  • The External jugular vein, Subclavian artery, and the brachial plexus are structures within this triangle.
  • Borders: sternomastoid muscle (clavicular head), trapezius, clavicle
  • Winds around the neck as it ascends from clavicle to lie behind the mastoid process.
  • Landmark deep within is the scalenus anterior
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12
Q

Describe the Anterior Triangle?

A
  • Lies in front, between the sternocleidomastoid and the midline of the body
  • Its base up along lower border of the mandible and its apex down at the suprasternal notch
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13
Q

What is the Position of transverse process of atlas?

A
  • Half way between mandible angle and the mastoid.

- This space also filled with parotid gland

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14
Q

What is the Hyoid bone?

A

The bone located in the neck between the mandible and the larynx, which supports the tongue and provides attachment for some of its muscles

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15
Q

What does the Sternocleidomastoid do?

A

Rotates head to opposite side and tilts ear to same shoulder

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16
Q

What does the Trapezius do?

A

Shrugs shoulders and extends neck

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17
Q

What are the 3 Major arteries passing from thorax?

A
  1. Right and left common carotid
  2. Brachiocephalic trunk
  3. Aortic arch
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18
Q

List the different head and neck veins?

A
  • Internal jugular vein
  • External jugular vein
  • Occipital vein
  • Retromandibular vein
  • Posterior external jugular vein
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19
Q

Common carotid

A
  • Landmark at lower end is sternoclavicular joint, line goes to transverse process of Atlas midway between mandible and mastoid.
  • Common bifurcates at C3/4 or upper edge of thyroid cartilage.
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20
Q

How to Palpate the Pulse of Carotid?

A
  • Line of common carotid
  • At or deep to anterior border of sternocleidomastoid, just above thyroid cartilage and below hyloid bone - picking up the common carotid bifurcation and the origins of both the internal and external carotids.
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21
Q

What are the Additional pulses of the head and neck?

A

Branches of the external carotid

  • Superficial temporal, anterior to the ear
  • Facial, crossing the mandible
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22
Q

What is the Jugular Venous Pulse Wave?

A

Increased atrial pressure due to filling against closed tricuspid valve

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23
Q

Describe the Internal jugular vein?

A
  • Sternoclavicular joint to TP atlas. Exits the skull from the jugular foramen, it lies posterior to the internal carotid artery.
  • Lateral to the artery for most of its course.
  • But is anterior to the artery at its termination.
  • Lies close to brachial plexus, phrenic nerves and vagus.
  • Can be accessed lateral to carotid artery but risky due to important structures nearby.
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24
Q

Describe the External Jugular vein?

A
  • Just below and behind angle of mandible to mid clavicle.
  • Verticle, superificial to sternocleidomastoid.
  • May be used for venous access, particularly in babies.
  • Pierces investing fasica and may be held open by it meaning theres a risk of air emboli.
  • Joins the subclavian vein
  • Carries blood returning to heart from head & neck
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25
Q

What are the Nerves of the neck?

A
  • Branches of the cervical plexus emerge posterior to sternocleidomastoid and pass adjacent to the external jugular
  • Accessory nerve passes across the posterior triangle to supply trapezius and sternocleidomastoid
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26
Q

What are the Lymph nodes of the neck?

A
  • Accompany external and internal jugular veins.
  • Drain the scalp, forehead, face, cheeks etc.
  • Superficial nodes drain to deep cervical nodes aligned with external jugular vein.
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27
Q

What does an Opthalmoscope do?

A
  • Study the retinal blood vessels.

- Very important in CVS examination.

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28
Q

What is another name for the coronary sulcus?

A

Atrioventricular groove

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29
Q

What are the only branches of the ascending aorta?

A

Coronary arteries

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30
Q

What is another name for the main stem artery?

A

Left coronary artery

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31
Q

What structures does the right coronary artery pass between?

A

Right auricle and pulmonary trunk

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32
Q

What branches does the right coronary artery give off?

A
  1. Marginal branch
  2. Posterior inter ventricular
  3. Nodal branch (suppling SA node)
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33
Q

What does the right coronary artery usually supply?

A
  • Walls of right atrium and right ventricle
  • Sinuatrial and atrioventricular nodes
  • Posterior interventricular septum
  • Proximal bundle of His
  • Small areas of left atrium and left ventricle
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34
Q

Which coronary artery is usually dominant?

A

Right coronary artery

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35
Q

What is an obstruction of the right coronary artery usually referred to as?

A

Inferior infarct- likely to case arrythmias

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36
Q

What structures does the left coronary artey pass between?

A

Arises between left auricle and Pulmonary trunk

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37
Q

What branches does left coronary artery give off?

A
  1. Circumflex branch, which divides to give the left marginal branch
  2. Anterior interventricular branch / LAD (left anterior descending)
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38
Q

What does the left coronary artery supply

A
  • Walls of the left atrium and left ventricle.
  • Most of the inter ventricular septum
  • Lower part of atrioventricular bundle.
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39
Q

Which artery is most commmonly affected by atherosclerosis?

A

LAD (artery of sudden death)

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40
Q

What vessel does an anterior infarct refer to?

A

Left anterior descending (LAD)

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41
Q

What vessel does a lateral infarct refer to?

A

Circumflex lateral

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42
Q

What does “CABG” stand for?

A

Coronary artery bypass grafting

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43
Q

What vessels are usually used in a coronary artery bypass?

A
  • left internal thoracic
  • internal mammary artery
  • great saphenous veins
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44
Q

What does “PTCA” stand for?

A

Percutaneous transluminal coronary angioplasty

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45
Q

Name the four cardiac veins going from right to left

A

Small cardiac vein –> anterior cardiac vein –> middle cardiac vein –> great cardiac vein

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46
Q

Which vein becomes the coronary sinus?

A

Great cardiac vein

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47
Q

What is the name of the veins draining directly into the chambers?

A

Venae cordis minimi

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48
Q

Where is the coronary sinus situated?

A

Between the left atrium and left ventricle, which empties into the right atrium

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49
Q

Where does the cardiac plexus lie?

A
  • Inferior to the arch of the aorta, adjascent to the bifurcation of the trachea.
  • Sends both afferent and efferent branches to the sinoatrial node, cardiac muscle and coronary arteries.
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50
Q

Which autonomic NS contribute to cardiac plexus?

A

Both sympathetic and parasympathetic

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51
Q

What type of tissue covers the endothelium of foetal capillaries in the placenta?

A

Syncytiotrophoblast

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52
Q

Which vessel brings oxygenated blood from the placenta?

A

Umbilical vein

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53
Q

Which vessels bring deoxygenated blood from the foetus?

A

2 Umbilical arteries

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54
Q

Which Vessels do the umbilical arteries branch from?

A

Internal iliac

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55
Q

What allows bypass of blood from right atrium to left? What circulation is being skipped?

A

Foramen ovale, pulmonary (SVC>RA>(FO)>LA)

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56
Q

Why in prenatal circulation is left atrial pressure very low?

A

Low pulmonary venous return, thus blood pulled in through foramen ovale

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57
Q

What vessel allows blood from the right ventricle to pass to the aorta? What circulation does this allow the blood to skip?

A

Ductus arteriosus, pulmonary (SVC>RA>RV>PY>Aorta)

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58
Q

How much blood bypasses the pulmonary circulation via ductus arteriosus?

A

90%

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59
Q

Where in the aorta does the ductus arteriosus join?

A

After the 3 branches to head/limbs

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60
Q

What is the purpose of the 10% of blood passing from the pulmonary trunk and entering the lungs?
(rather than passing through the ductus arteriosus)

A

Supplies developing foetal lungs

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61
Q

What compound is responsible for the patency of the ductus arteriosus?

A

Prostaglandins

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62
Q

Which vessel allows foetal blood to bypass the liver?

A

Ductus venosus

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63
Q

How much blood bypasses the liver?

A

50%

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64
Q

Where does the ductus venosus insert?

A

Inferior vena cava

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65
Q

Which blood is the most highly oxygenated?

A

Blood in IVC, so passes through foramen ovale to left ventrical and systemic circulation

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66
Q

What causes the foramen ovale to close?

A

First breath pulls blood into lungs, venous return to LA increases intratrial pressure, which equalizes with right atria and causes the foramen ovale to close

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67
Q

How is the ductus arteriosus obliterated?

A
  • Initial smooth muscle constriction, 02 tension increases, 02 potent constrictor of DA.
  • Placenta stops producing prostaglandins, which are removed from circulation by the functioning lungs.
  • Later anatomical closure through thickening of tunica intima
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68
Q

What is the postnatal remenant of the ductus arteriosus?

A

Ligamentum arteriosum

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69
Q

What happens in patent ductus arteriosus?

A

Aortic pressure is greater than in the pulmonary trunk, so blood will flow back into the pulmonary trunk causing pulmonary hypertension and congestive cardiac failure.

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70
Q

How is the ductus venosus obliterated?

A
  • Umbilical vessels contract with the delivery of the placenta, postnatal hepatic circulation is established and the ductus venosum becomes the ligamentum venosum.
  • The umbilical vein becomes ligamentum teres
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71
Q

What is the name for the formation of a trilaminar disk?

A

Gastrulation

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72
Q

What are the three layers of the trilaminar disc?

A
  1. ectoderm
  2. mesoderm
  3. endoderm
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73
Q

Which embryonic tissue does the heart tube form from?

A
  • Mesoderm

- Forming angiogenetic clusters

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74
Q

Where does the heart tube form?

A

In a horse shoe shape at the cephalic end of the trilaminar disk

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75
Q

When does cephalo-caudal folding start?

A

18th day (end of 3rd week)

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76
Q

What development of the heart tube results from the folding?

A

Lateral folding swings the two limbs of the horseshoe medially, so they fuse as a single heart tube

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77
Q

When does looping and folding occur?

A

22 days (early week 4)

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78
Q

Which way do the two ends of the heart tube fold towards?

A
  • To the right, so pushing the apex to the left.

- Rotating slightly so that the right side of the heart tends to be more anterior

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79
Q

What are the two main causes of heart defects?

A
  1. Genetic causes

2. Teratogenic causes

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80
Q

Why are craniofacial abnormalities linked to heart defects?

A

Also use neural crest cells for development

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81
Q

Why can early embryonic development be sustained without a heart?

A

Diffusion is sufficient due to surface area:volume ratio

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82
Q

What additional embryonic tissue is formed in week three during gastrulation?

A

Mesoderm- will go on to form heart tissue

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83
Q

What is Dextrocardia?

A

Cardiac folds to the left, resulting in the heart being pushed to the right

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84
Q

What developments occur at 28 days?

A

Developing heart pushes into the pericardial sac, ventricles begin to trabeculate

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85
Q

What does the bulbus cordia form?

A

Mid portion forms the conus cordia which will form the conus portion which will from outflow tracts. The proximal part will form the right ventricle, the distal part will from the trunks of the great vessels

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86
Q

What vessels does the venous end of the heart tube receive?

A

Cardinal, umbilical and vitelline veins.

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87
Q

Where are the veins flowing into the heart tube in relation to the arteries running out?

A

Posterior- opposite to postnatal heart

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88
Q

What cells are endocardial cushions derived from?

A

Neural crest cells

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89
Q

What structures in the heart are derived from the endocardial cushion cells?

A

Interatrial septum, the membranous part of the interventricular septum, the atrioventricular valves, the formation of the aorta and pulmonary trunk from the truncus arteriosus

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90
Q

Which chambers are divided first?

A

Left and right side of the heart separate into 2 atrioventricular canals (left=mitral, right =tricuspid)

91
Q

What is the first septum to form between the atria?

A

The septum primum growing in the interatrial ostium primum, this grows towards the developing endocardial cushion which has just separated the two atrioventricular canals

92
Q

What is the 2nd septum to form between the atria?

A

Septum secundum grows, as tiny holes develop in the developing septum primum, which allow blood flow, the holes are called the ostium secundum. A hole forms in the developed septum secundum called the foramen ovale

93
Q

When does atrial septation occur?

A

Weeks 5 & 6

94
Q

When is the formation of the interventricular septum complete?

A

By the end of week 7

95
Q

What are the 4 components of the ventricular septum?

A

Endocardial cushions form left and right endocardial ridges,
extension of inf. endocardial cushion produced the membranous part of the interventricular septum,
Proliferation of ventricular muscle forms the muscular part of the septum,
left and right truncal ridges from the conotruncal spetum

96
Q

What is Fallots tetralogy?

A

Truncal septum deviates to the right and does not meet the interventricular septum

97
Q

How are the mitral and tricuspid valves formed?

A

Endocardial cushion growth and cavitation to form papillary muscles and chordae tendinae

98
Q

Which dorsal arch forms the maxillary arteries?

A

1st arch (left and right)

99
Q

Which dorsal artery forms the common carotid arteries?

A

3rd arch (with dorsal aorta)

100
Q

Which dorsal arch from the arch of the aorta?

A

Left 4th arch

101
Q

Which dorsal arch forms the right subclavian?

A

Right 4th arch

102
Q

Which dorsal arch forms the pulmonary trunk?

A

Left 6th arch (right 6th also contributed)

103
Q

What is Coarctation of the aorta?

A

Narrowing after the origin of the left subclavian dues to abnormality in the aortic media and intima proliferation

104
Q

What happens as result of coarctation of the aorta?

A

Blood travels in subclavian to the internal thoracic arteries, to intercostal vessels and back to the thoracic aorta (FEMORAL PULSES WILL BE WEAK)

105
Q

What nerve do recurrent laryngeal nerves originate from?

A

Vagus nerve

106
Q

Where and why does recurrent laryngeal nerve sit on the left?

A

6th arch, so hooks under aorta and is held by ductus arteriosus

107
Q

Where and why does the recurrent laryngeal nerve sit on the right?

A

5th and 6th arches regress on the right, so hooks under 4th arch- the right subclavian artery

108
Q

Functional Syncitium

A
  • Cells of atrial myocardium are all electrically connected
  • Depolarise and contract synchronously
  • Ventricles are similar but are a separate functional unit
109
Q

Cardiac skeleton

A
  • Connective tissue between atria and ventricles, prevent flow of electrical current between the two.
  • Atria and ventricles electrically separate except at AV node
110
Q

Conduction Network

A

1% of cardiac fibres dont contract, but form the excitatory and conductive muscle fibres

111
Q

Pacemaker activity

A
  • SAN is the intrinsic pacemaker

- Other areas have pacemaker ability

112
Q

Autonomic innervation

A
  • Sympathetic nerves INCREASE the rate of SAN depolarisation

- Parasympathetic nerves DECREASE the rate of SAN depolarisation

113
Q

What is the Plateau phase?

A
  • 2nd phase
  • Balance of K+ ions flowing out of the cell against the influx of Ca2+ flowing in.
  • When the intracellular calcium concentration reaches a certain level, more K+ channels open and the L-type Ca2+ channels close to cause phase 3.
  • Prevents tetany from occuring.
114
Q

Describe the phases in Atrial/ventricular depolarisation?

A

PHASE 0 -Rapid depolarisation due to increase in Na permeability as fast Na channels open up
PHASE 1 -Once reach 20mV Na channels close causing drop in Na permeability. Start of repolarisation
PHASE 2 -Effect of Ca entry via L-type channels. Keeps cell in depolarised state - plateau region.
PHASE 3 -Rapid repolarisation as increase in Ca stimualtes K channels to open and K permeability to increase. Ca L-type channels close
PHASE 4 -Stable resting membrane potential where gK exceeds gNa by 50:1

115
Q

Describe the phases in SA node depolarisation?

A

PHASE 1 - Gradual increase in resting potential due to ‘funny’ F-type Na channels open and K channels slowly close. Transient (T) Ca channels help with the final push
PHASE 2 - Moderately rapid depolarisation due to Ca entry via slow L channels.
PHASE 3 - Rapid repolarisation as elevated internal Ca stimulates opening of K channels. As potential becomes more negative F-type Na channels start to open, preventing return to resting potential and starting gradual creep towards threshold potential.

116
Q

What is a Pacemaker potential?

A
  • A self-induced slow depolarization to threshold occurring in a pacemaker cell as a result of shifts in passive ionic fluxes across the membrane accompanying automatic changes in channel permeability.
  • Gradual creep caused by the F-type Na+ channels.
117
Q

What are F-type (“funny” type) voltage-gated Na channels?

A

“Funny” because they open as the membrane voltage becomes more negative, which is different from normal voltage- gated Na+ channels which open when the membrane potential becomes more positive.

118
Q

Describe the Autonomic nervous system?

A
  • Sympathetic controls whole heart (myocardial tissue). Can act as accelerator of heart through muscle fibres themselves. Effect on speed and force of contraction
  • Parasympathetic controls node tissue only. Only going to affect nodal tissue so can only affect speed of contraction.
119
Q

Describe Sympathetic stimulation?

A
  • Noradrenaline acts on B1 receptors to increase cAMP production
  • This increases the rate of SAN phase 1 depolarsation by increasing gCa through slow channels and increasing gNa via funny channels
120
Q

Describe Parasymapthetic stimulation?

A
  • Acetylcholine on M2 receptors which decreases cAMP production
  • Reduces rate of phase 1 depolarisation
  • Hyperpolarises membrane potential to lower starting level by increasing the extent and duration of opening of the K channels and therefore increasing gK.
121
Q

What is Positive chronotropic effect?

A
  • Increased heart rate

- Shown by sympathetic stimulation

122
Q

What is Negative chronotropic effect?

A
  • Slowed heartbeat

- Shown by parasympathetic stimulation

123
Q

Describe the SA node?

A
  • Located in the top of the right atrium just below superior vena cava
  • Starts the heart beat by sending an electrical impulse through the atria.
  • Has the fastest rate of the heart elements so is the intrinsic pacemaker.
  • Depolarisation spreads from SAN throughout the heart before other regions spontaneously depolarise.
  • If conduction blocked, downstream tissues assume their intrinsic rate.
124
Q

Describe the AV node?

A
  • Located at the posterior septal wall at the right atrium just above the tricuspid valve
  • Atrioventricular region of the heart between the right atrium and right ventricle from which electrical impulses spread to the ventricles during a heartbeat
125
Q

What is “Bundle of His”?

A

A collection of heart muscle cells specialized for electrical conduction that transmits the electrical impulses from the AV node (located between the atria and the ventricles) to the point of the apex of the fascicular branches via the purkinje fibres

126
Q

What is “Purkinje fibres”?

A
  • Fastest path of conduction in heart
  • Divisions of the Bundle of His that reach deep into the endocardium and produce a simultaneous contraction of the ventricles from the bottom up.
127
Q

What are the 5 different Intrinsic rates of the heart?

A 
SAN - 90/min
AV node - 60/min
Bundle of his - 50/min
Purkinje fibers - 40/min
Ventricles - 30/min
128
Q

What is Einthoven’s triangle?

A
  • The placement of electrodes (in an ECG) on the body forms a triangle.
  • Measure electrical activity between points on the triangle
    Size of electircal signals from the heart is determined by:
    -current (proportional to tissue mass)
    -Direction of signal
129
Q

What is the equation for the Actual electrical signal?

A

Observed signal = E x cosO

  • Smallest angle gets biggest observed signal
  • The more parallel you are to the activity the closer you are to signal
130
Q

What does the Electrocardiogram (ECG) do?

A

Takes a recording of the electrical activity of the heart

131
Q

What is the reason of the different waves in an Electrocardiogram graph?

A

P wave- atrial depolarisation
QRS wave- ventricular depolarisation
T wave- Ventricular repolarisation

132
Q

What ion channel is responsible for propagating the AP in cardiac muscle?

A

Voltage gated sodium

133
Q

What channels open as a result of the AP propogating down in the T Tubules?

A

L-type dihydropyridine calcium channels

134
Q

Where does calcium move from through L type channels?

A

Outside the cell

135
Q

What percent of the calcium moving through the L type calcium channels contributes to cardiac contraction?

A

10%

136
Q

What is responsible for the high concentration of calcium in the T Tubules?

A

Mucopolysaccharides that sequester Ca2+

137
Q

How many times greater is the cardiac T-tubule volume compared to skeletal?

A

25x more volume (5 times greater diameter)

138
Q

What channels in the sarcoplasmic reticulum allow the calcium spark?

A

Ryanodine release channels (calcium induced calcium release)

139
Q

Which pump affected by sympathetic Stimulation?

A

Calcium ATP pump on sarcoplasmic reticulum membrane= pumps more Ca++ into sarcoplasmic R. so more is ready to be released on the next stimulation. Thus more powerful contraction

140
Q

What is Preload?

A

Venous pressure and venous return to the heart (end diastolic pressure)
(ALWAYS THE SAME, REGARDLESS OF CARDAIC OUTPUT)

141
Q

What is cause of the refractory period?

A

Inactivation of voltage gated sodium channels

142
Q

What is the cause of repolarisation?

A

Closure of L-type calcium channels, and sudden opening of potassium channels

143
Q

Length of AP in Cardiac muscle?

A

245ms

144
Q

What is the Period of contraction of cardiac muscle?

A

250ms

145
Q

What is SNP?

A
  • Supranormal period of excitability

- Requires less than normal sized stimulus to activate

146
Q

How much of ventricular filling is passive?

A

80%

147
Q

how quickly is the first 70% ejected from ventricles

A
  • RAPID

- First 1/3

148
Q

Isovolumic

A

No change in blood volume in chambers, valves closed

149
Q

How do you calculate the Stroke volume (SV)?

A

end diastolic volume - end systolic volume

EDV - ESV

150
Q

What is the end systolic volume (ESV)?

A

Volume in ventricle at end of sytole

151
Q

What is the End diastolic volume (EDV)?

A

Volume in ventricle at the end of diastolic

152
Q

What is the range in stroke volume that the heart can achieve?

A

70-140ml

153
Q

What is the range in heart rate the heart can achieve?

A

70-200bpm

154
Q

What is the range in cardiac output that the heart can achieve?

A

5-30 (L/min)

155
Q

What is Afterload?

A

Force exerted by pulmonary artery/aorta (needs to be overcome in order to expel blood from ventricles)

156
Q

What is the main intrinsic mechanism regulating stroke volume?

A

Frank Starling mechanism

157
Q

What is the main extrinsic mechanism regulating stroke volume?

A

Sympathetic innervation

158
Q

Which mechanism allows for automatic adjustment for small imbalances between left and right ventricular stroke volume?

A

Frank Starling mechanism

159
Q

Does the Frank Starling Mechanism work in addition to inotropic stimulation of heart?

A

YES

160
Q

Cardiac output=

A

Stroke volume (SV) x heart rate (HR)

161
Q

Arterioles have a ___ capacity

A

Low

162
Q

Arterioles have a ____ resistance

A

High

163
Q

Venous system has a ____ capacity

A

High

164
Q

Venous system has a ___ resistance

A

Low

165
Q

What is Compliance?

A

Degree to which a vessel can expand on the onset of pressure

166
Q

High compliance

A

Small change in pressure results in large change in diameter

167
Q

Compliance can be reduced by what 2 things?

A
  1. Vasoconstriction

2. Age

168
Q

What does “MABP” Stand for?

A

Mean arterial blood pressure

169
Q

MABP=

A

Diastolic pressure + 1/3 pulse pressure

170
Q

Poiseulle equation flow =

A

Flow= change in pressure/ resistance

171
Q

Arterial pressure=

A

cardiac output x total peripheral resistance

172
Q

What 3 Factors determining magnitude of pulse pressure?

A
  1. Stroke volume
  2. speed of ejection
  3. arterial compliance
173
Q

What shape does the velocity profile of blood take in a vessel during lamina flow?

A

Parabolic (due to friction between endothelial blood vessel cells and blood cells)

174
Q

What happens in Reynold’s number is exceeded?

A

Experience turbulence

175
Q

Reynolds number (Re)=

A

(Velocity of flow) x (radius of vessel)/viscosity

176
Q

name 4 factors increasing turbulence

A
  1. High velocity flow
  2. large diameter vessels
  3. increased viscosity blood
  4. abnormal vessel wall
177
Q

Thixotropic

A
  • Flow affects viscosity of fluid

- static blood solidifies

178
Q

What is LaPlace’s law?

A

Distending pressure(P) produces an opposing force or tension (T) in the vessel wall, proportional to the radius of the vessel (R)

T= PR

179
Q

How does Laplace’s law affect aneurysms?

A

Weakening causes increase in radius of vessel, which in turn results in an increased tension in the vessel, which will further the vessel wall weakening and so further the distention

180
Q

What are Metarterioles?

A

Links arterioles to venules, made of discontinuous smooth muscle, capillaries branch off.

181
Q

What are Arterioles job?

A

Control regional distribution (local and extrinsic controls)

182
Q

What are Precapillary sphincters?

A

Found where a true capillary branches from a metarteriole, vasodilate according to build up of local factors which results in increased blood flow to that capillary bed

183
Q

What is the arteriole response to an increase in pressure in flow auto regulation?

A

Constriction to reduce flow

184
Q

What is the arteriole response to a decrease in pressure in flow auto regulation?

A

Dilate to increase flow

185
Q

What is the myogenic response in blood vessels to an increased pressure (part of autoregulation)

A
  • Stretch activates Ca”+ channels open, resulting in a depolarization and contraction on the smooth muscle in arterioles.
  • resulting in constriction
186
Q

What potent vasoconstriction factor is released upon tissue injury?

A

Endothelin-1

187
Q

What is Active hyperemia?

A

Rate of flow increasing due to active tissue (up to 20s increase in skeletal muscle)

188
Q

What is Reactive hyperemia?

A

Blood supply blocked, resulting in build up of factors, resulting in a signal to increase blood flow (4-7x increase)

189
Q

Which autonomic nervous system is responsible for vasoconstriction?

A

Sympathetic

190
Q

Which 3 hormones bring about vasoconstriction?

A
  1. adrenaline
  2. Angiotensin II
  3. vasopressin
191
Q

Which 2 local responses bring about vasoconstriction?

A
  1. Myogenic response

2. endothelin-1

192
Q

Which 2 hormones bring about vasodilation?

A
  1. Adrenaline (skeletal muscle)

2. Atrial-Natriuetic peptide

193
Q

What controls the vasodilation of the sexual organs?

A

NO releasing parasympathetic nerves

194
Q

Which local factors affect vasodilation?

A

Mainly Adenosine, also increased K+, CO2, H+, NO, Histamine, and decreased O2

195
Q

At rest, what percent of cardiac output is in capillaries?

A

~5%

196
Q

What changes are described as long term regulation of blood flow?

A

Change in size or number of blood vessels

197
Q

Which vessels have slowest velocity blood?

A

Capillaries- allow time for diffusion

198
Q

What are Viruses?

A
  • Small infective agents consisting of nucelic acid (RNA or DNA) enclosed in a protein coat.
  • Not cells as have no metabolic machinery of their own, are obligate intracellular parasites
199
Q

What is an Obligate?

A

An organism that requires oxygen for cellular respiration and cannot live without it

200
Q

What is a Capsid?

A
  • The protein shell that encloses a viral genome.

- It may be rod-shaped, polyhedral, or more complex in shape

201
Q

What is SS RNA?

A
  • Single stranded RNA viruses are classified as positive or negative depending on the sense or polarity of the RNA.
202
Q

2 Examples of DS DNA?

A
  • Herpes virus

- Adenovirus

203
Q

Example of SS DNA?

A

Parovirus

204
Q

Example of +SS RNA?

A

HIV

205
Q

2 Examples of -SS RNA?

A
  • Arenavirus

- Rhabdovir

206
Q

Describe Virus Replication?

A
  • In order to replicate they have to attach to and enter a living host cell and use its metabolic processes.
  • The binding sites on the virus are polypeptides on the envelope or capsid
  • The receptors on the host cells, to which the virus attaches, are normal membrane constituents
  • With many viruses, the receptor virus complex enters the cell by receptor-mediated endocytosis during which the virus coat may be removed. Some bypass this route.
  • Once in the host cell, the nucleic acid of the virus then uses the cells machinery for synthesising nucleic acid and protein and the manufacture of new virus particle
207
Q

List the 8 different Types of antiviral drugs?

A
  1. Entry inhibitor
  2. Viral Uncoating
  3. Nucleoside analogue chain termination
  4. NNRTIs (non-nuceloside reverse transcriptase inhibitors)
  5. Protease inhibitors
  6. Integrase Inhibitors
  7. Virus Release Inhibitors
  8. Immunomodulator
208
Q

What is the Virus Life Cycle?

A
  1. Recognition
  2. Attachment
  3. Penetration
  4. Uncoating
  5. Transcription
  6. Protein synthesis
  7. Replication
  8. Assembly
  9. Lysis and release
209
Q

Nucleoside analogues

A
  • Inhibit replication of HIV virus by inhibiting the transcription of RNA and DNA.
  • Inhibit synthesis of nucleic acids (binding to the viral DNA polymerase and preventing viral DNA replication)
210
Q

Protease inhibitors

A

Prevent viral replication by selectively binding to viral proteases and blocking proteolytic cleavage of protein precursors that are necessary for the production of infectious viral particles.

211
Q

DNA viruses

A

Eg. HSV, HPV
There is generally entry of the viral DNA into the host cell nucleus
Transcription of this viral DNA into mRNA by host cell RNA polymerase followed by translation of the mRNA into virus-specific proteins

212
Q

How do you treat Cytomegalovirus (CMV)?

A
  • Acyclovir not as active

- Treat with ganciclovir and valganciclovir

213
Q

RNA viruses

A

Eg. Influenza (flu), Hep C (HCV)
RNA viruses classified according to the sense or polarity of their RNA
Positive-sense viral RNA is similar to mRNA and can be immediately translated by the host cell
Negative-sense RNA is complementary to mRNA and must be converted to positive-sense by RNA polymerase before translation
RNA polymerase directs the synthesis of more viral genomic RNA
Typically virus replication occurs in the host cell cytoplasm not the nucleus

214
Q

Retroviruses

A

Eg. HIV, Human T cell Leukemia Virus (HTLV)
Virus contains reverse transcriptase an RNA-dependent DNA polymerase, which makes a DNA copy of the viral RNA.
This DNA copy is integrated into the genome of the host cell and it is then termed a provirus
The provirus DNA is transcribed into both new genomic RNA and mRNA for translation into viral proteins using host cell machinary.
Some RNA retroviruses can transform normal cells into malignant cells.

215
Q

HIV structure

A 
GP-120 is a grabber for the HIV. Grabs onto the Macrophages/t cells. Conformation happens and then its allowed to bind to a coreceptor- either CCR5 or CXCR4 = tropism- important for therapy. Dual tropism = HIV that can bind to either CCR5 or CXCR
Nucleic acid (RNA) surrounded by core proteins, which in turn are surrounded by a capsid (protein shell), which in turn is surrounded by a lipid bilayer envelope
216
Q

Approved Antiretroviral Drugs

A 
Reverse Transcriptase Inhibitors
Protease Inhibitors
Early Inhibitors
Fusion Inhibitors
Integrase Inhibitors
>25 different drugs, 6 different mechanistic classes
217
Q

Reverse transcriptase inhibitor

A

When HIV infects a cell, reverse transcriptase copies the viral single stranded RNA genome into a double-stranded viral DNA. The viral DNA is then integrated into the host chromosomal DNA, which then allows host cellular processes, such as transcription and translation, to reproduce the virus. RTIs block reverse transcriptase’s enzymatic function and prevent completion of synthesis of the double-stranded viral DNA, thus preventing HIV from multiplying.
A similar process occurs with other types of viruses. The hepatitis B virus, for example, carries its genetic material in the form of DNA, and employs a RNA-dependent DNA polymerase to replicate.

218
Q

Nucleoside/nucelotide analogues

A

Compete with the natural substrate (dNTPs for DNA synthesis or NTPs for RNA synthesis) in DNA or RNA polymerization, therefore virus specific selectivity
Act as chain terminators by not offering the 3′-hydroxyl function at the (2′-deoxy)riboside moiety, which is required for attachment of the incoming nucleotide.
Or nucleotide analogues possessing an hydroxyl function at a position
equivalent to the 3′-hydroxyl position act as chain terminator if this hydroxyl group
is conformationally constrained and therefore hinders attachment of the incoming nucleotide.
They are prodrugs and require intracellular phosphorylation by viral and/or cellular kinases to convert them from the 5’-monophosphate form to 5’-triphosphates.

219
Q

Protease Inhibitors

A

Host mRNAs code directly for functional proteins
In HIV, mRNA is translated into biochemically inert proteins
A virus-specific protease then converts them into various functional proteins
Since the protease does not occur in the host, it is a good selective-toxicity target

220
Q

Integrase

A

HIV integrase mediates 2 critical reactions:

  1. 3’ end processing of the double stranded viral DNA ends
  2. Strand transfer which joins the viral DNA to the host chromosomal DNA forming a functionally integrated provirus
221
Q

Integrase Inhibitors

A

For HIV resistant to other HAART regimanes
Medications that interrupt the viral replication cycle by inhibiting integrase enzymes that allow the transcribed viral DNA to integrate into the host cell DNA

222
Q

Fusion inhibitors

A

Entry of HIV into a new cell is mediated by the Env glycoprotein spike a trimer of pg120 and gp41. Entry requires the receptor CD4 plus on eof 2 receptors, CCR5 or CXCR4

223
Q

Neuraminidase

A

Functions in influenza infection by cleaving sialic acid from the cell surface so that newly made viruses are released and able to spread to uninfected cells

MD3001 (15 decks)

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