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MD3001 > WEEK 1 > Flashcards

WEEK 1 Flashcards

1
Q

The neck is essentially composed of vertical columns surrounded by fascial sheets with potential spaces between. Describe the columns & fascia in detail.

A
  1. Neuro-musculo-skeletal column with prevertebral (base of skull to ligs at T3) fascia 2. Visceral column with pretracheal (from hyoid to fuse with pericardium) & buccopharygeal fascia 3. Carotid NVB with carotid sheath on each side Everything is surrounded by the layer of INVESTING FASCIA (which splits to enclose trapezius & sternocleidomasteoid muscle)
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2
Q

Describe the concept of the anterior and the posterior triangles of the neck, and their boundaries

A
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3
Q

Where do the internal & external carotid arteries begin & end? Where does the common carotid bifurcate?

A

sternoclavicular joint to the transverse process of the atlas (midway between mastoid & angle of mandible)

at C3/4 or the upper edge of thyroid cartilage

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4
Q

Where is the internal jugular vein found?

A

deep to sternocleidomastoid, but superficial to the common and internal carotids - therefore visible as the (raised) jugular venous pulse wave

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5
Q

Where is the (i) cutaneous cervical plexus (ii) accessory nerve located? What does the accessory nerve supply?

A

Emerging posterior to sternocleidomastoid and passing adjacent to the external jugular vein

passing across the posterior triangle to supply trapezius

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6
Q

What are the internal & external jugular veins accompanied by?

A

Superficial & deep cervical lymph nodes

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7
Q

What is the path of the internal jugular vein - with reference to the internal carotid artery.

A

As the IJ Vexits the skull from the jugular foramen, it lies posterior to the internal carotid artery

It is then lateral to the artery for most of its course

But is anterior to the artery at its termination

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8
Q

Where is the external jugular located? What is it used for?

A

Just below & behind the angle of the mandible, to mid clavicle

more or less vertical, superficial to sternocleidomastoid

May be used for venous access (particuarly in babies)

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9
Q

What is meant by the term “functional syncitium”?

A

Cells of atrial myocardium are all electrically connected. They depolarise & contract synchronously.

The ventricles have a similar structure but are a separate functional unit

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10
Q

What is the process of electrical conduction at intercalated discs and the principles resulting in “pacemaker” activity?

A

About 1% of cardiac fibres do not contract, but form the excitatory & conductive muscle fibres

SAN = the intrinsic pacemaker , BUT other areas do have pacemaker ability

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11
Q

With regards to SAN depolarisation, what does (i) sympathetic (ii) parasympathetic nerves do to its rate?

A

(i) increases rate of SAN depolarisation
(ii) decreases rate of SAN depolarisation

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12
Q

Describe the 5 phases involved in atrial/ventricular depolarisation. (HINT: THE FIRST IS PHASE 0)

A

PHASE 0 - rapid depolarisation due to an increase in Na permeability (gNa) as fast Na channels open

PHASE 1 - start of repolarisation as fast Na channels close

PHASE 2 - effect of Ca entry via L-type channels

PHASE 3 - rapid repolarisation as increase in intracellular Ca stimulates K channels to open & gK increases. Ca L type channels close

PHASE 4 - stable resting membrane potential where gK exceeds gNa by 50:1

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13
Q

What are the 3 phases of SAN depolarisation? Describe them.

A

PHASE 1 - a gradual drift increasing in resting membrane potential due to an increase in gNa as “funny” F-type Na channels open & decreases gK permeabiility as K channels slowly close. “pacemaker potential”. 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 an opening of K channels and an increase in gK

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14
Q

How do the sympathetic and parasympathetic nerves modify the spontaneous electrical activity of the heart?

A

SYMPATHETIC: NA acts on beta1 receptors to increase cAMP production. It increases the rate of SAN phase 1 depolarisation, which increases gCa & gNa “funny” channels

SHOWS +VE CHRONOTROPIC EFFECT

PARASYMPATHETIC: ACh on M2 receptors which decreases cAMP production . It reduces the rate of phase 1 depolarisation. Hyperpolarises membrane potential to lower starting level which increases the extent & duration of opening of potassium channels which increases gK

SHOWS -VE CHRONOTROPIC EFFECT

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15
Q

What are the rates of depolarisation of (i) SAN (ii) AV node (iii) Bundle of His (iv) Purkinje fibers (v) Ventricles?

A

(i) 90/min
(ii) 60/min
(iii) 50/min
(iv) 40/min
(v) 30/min

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16
Q

What is the intrinsic pacemaker?

A

The SAN as it has the fastest rate

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17
Q

What happens if conduction is blocked?

A

Downstream tissues assume their intrinsic rate

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18
Q

What does an Electrocardiogram (ECG) measure? How many electrodes are used and where?

A

Measures electrical activity of the heart over time

Uses multiple electrodes:

  • 4 on the limb : ones an “earth”, used to remove background noise noise & the other 3 are used to create virtual “leads” between each pair of electrodes
  • 6 across the chest: to give more sepcific, localised information about areas of the heart
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19
Q

What 2 things do the limb leads measure? What causes the trace to go (i) up (ii) down?

A

They measure the sum of the electrical activity of the heart & the direction that the electrical activity is moving in

  • one end of each lead is designated “positive”

depol moving TOWARDS the positive causes the trace to go UP

depol moving AWAY from the positive causes the trace to go DOWN

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20
Q

What 2 things determine the size of electrical signals from the heart?

A

current (proportional to tissue mass)

direction of signal

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21
Q

What is the equation for calculating the observed signal? Explain what each symbol stands for.

A

Observed signal = E x Cos (theta)

the smallest angle gets the biggest observed signal

E = electrical event

theta = angle between the event & ECG lead

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22
Q

With regards to an electrocardiogram, what is the (i) P wave (ii) QRS wave (iii) T wave?

A

(i) atrial depolarisation
(ii) ventricular depolarisation
(iii) ventricular repolarisation

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23
Q

What are the timing intervals for (i) P-R interval (ii) QRS complex width (iii) Q-T interval?

A

(i) 0.15 - 0.2s
(ii) 0.08 - 0.12s
(iii) 0.25 - 0.35

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24
Q

How is force is produced in cardiac muscle? How does this differ from skeletal muscle?

A

An AP causes L-type dihydropyridine channels to open resulting in a large influx of calcium from outside of the cell (only about 10% of this contributes to contraction)

Cardiac muscles T tubules are 5x greater in diameter than skeletal (=> 25x greater volume)

Cardiac t-tubule mucopolysaccharides sequester Ca2+

DHP activation causes release of Ca from sarcoplasmic reticulum via ryanodine release channels

At resting HRs, intracellular Ca conc increases due to influx & sarcoplasmic release is insufficient to cause maximal contractile force ( heart at sub optimal conditions)

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25
Q

How do the extrinsic sympathetic nerves increase force production by direct effects on calcium availability?

A

Sympathetic innervation causes a positive ionotropic effect throughout the entire heart

NA on beta1 receptors which:

  • increases cAMP intracellularly
  • enhances Ca influx
  • therefore increasing contractility & the speed of relaxation
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26
Q

What is the duration of atrial & ventricular contraction in cardiac muscle?

A

Cardiac muscle begins to contract a few milliseconds after the action potential begins and continues to contract until a few milliseconds after the action potential ends. Therefore, the duration of contraction of cardiac muscle is mainly a function of the duration of the action potential, including the plateau—about 0.2 second in atrial muscle and 0.3 second in ventricular muscle.

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27
Q

How do the extrinsic parasympathetic nerves reduce force production by indirect means?

A

Mostly to the SA node

Innervates atria

Its main effect is decreasing the rate but it also has an indirect -ve ionotropic effect

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28
Q

Why can’t cardiac muscle be tetanised?

A

Because of the long refractory period of the muscle, during which it does not respond to stimulus.

The refractory period is due to inactivation of the Na channels

Cardiac muscle

– Absolute refractory period (ARP) ~245ms

– Relative refractory period (RRP)

– Period of supranormal excitability (SNP)

– Period of contraction 250ms

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29
Q

Recall the details of the timing of the electrical and resulting mechanical events of the cardiac cycle.

A

Atria as primer pumps

– ~80% of ventricular filling is passive due to normal blood flow – Atrial contraction ‘tops up’ remaining ~20% volume

Ventricles as pumps

– Isovolumic (isometric) period of contraction

– Period of rapid ejection (1/3) when 70% of stroke volume

ejected

– Period of slow ejection (2/3) when remaining 30% ejected

– Isovolumic (isometric) period of relaxation

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30
Q

What does the force production in the heart involve?

A

all myocardial fibres in every beat

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31
Q

What is the systolic BP in the (i) aorta (ii) pulmonary circulation?

What is the diastolic BP in the (i) aorta (ii) pulmonary circulation?

A

(i) 120 mmHg
(ii) 80 mmHg
(i) 30 mmHg
(ii) 12mmHg

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32
Q

Why is pressure in the pulmonary circulation much lower than in the aorta?

A
  • Much less resistance to flow
    – Right side of heart needs to do less work
    – Right ventricle walls contain less muscle mass
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33
Q

What is the (i) ESV (ii) EDV (iii) SV (iv) CO?

A

(i) END SYSTOLIC VOLUME = volume in the ventricle at the end of systole
(ii) END DIASTOLIC VOLUME = volume in the ventricle at the end of diastole
(iii) STROKE VOLUME = EDV - ESV, the quantitiy of blood expelled per beat (L)
(iv) CARDIAC OUTPUT = SV x HR , volume of blood pumped by the heart (L/min)

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34
Q

What factors contribute to changes in cardiac output? Describe them.

A

(1) the basic level of body metabolism
(2) whether the person is exercising
(3) the person’s age
(4) size of the body.

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35
Q

What is the Frank-Starling law of the heart?

A

when increased quantities of blood flow into the heart, the increased blood stretches the walls of the heart chambers. As a result of the stretch, the cardiac muscle contracts with increased force, and this empties the extra blood that has entered from the systemic circulation. Therefore, the blood that flows into the heart is automatically pumped without delay into the aorta and flows again through the circulation

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36
Q

An increase in EDV results in an increase in what?

A

Force of contraction

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37
Q

How is cardiac output increased in response to increased demand?

A
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38
Q

Define inotropic.

A

Modifying the force or speed of contraction of muscles.

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39
Q

What is a chronotropic effect? What does (i) positive chronotropes (ii) negative chronotropes do to heart rate?

A

Chronotropic effects are those that change the HR, they may change the HR & rhythm by affecting the electrical conduction system of the heart & the nerves that influence it (e.g. changing the rhythm produced by SAN)

(i) increase HR
(ii) decrease HR

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40
Q

What are the (i) intrinsic & (ii) extrinsic controls of stroke volume?

A

(i) self regulation

frank-starling mechanism

increased EDV => increased contraction force

(ii) sympathetic nerves

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41
Q

What is the Poiseuille relationship?

A

Poiseuille Equation: Flow = delta P / resistance

Arterial pressure = cardiac output x total peripheral resistance

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42
Q

What is MABP? How is it calculated?

A

Mean arterial blood pressure

diastolic pressure + 1/3 pulse pressure**

** pulse pressure = systolic pressure - diastolic pressure

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43
Q

What factors determine the magnitude of pulse pressure?

A
  1. STROKE VOLUME: intrinsic & extrinsic factors. Remember afterload, preload, sympathetic innervation
  2. SPEED OF EJECTION OF STROKE VOLUME
  3. ARTERIAL COMPLIANCE: decreases with age (arteriosclerosis)
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44
Q

What is the difference between streamline & turbulent flow? What type of flow is blood normally?

A

STREAMLINE (laminar) - vessels are lined with endothelial cells. The fluid molecules touching wall move slowly, & the middle most layer moves the fastest

TURBULENT - when flow is disrupted & does not go in the right direction, resistance increases.

It’s normally streamlined

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45
Q

What is Reynolds number used to indicate? What is the equation?

A

Whether flow is likely to be laminar or turbulent - For a given system, there will be a “critical value” for Re, above which turbulence is highly likely

Re = (velocity of flow) x (radius of vessel) / viscocity

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46
Q

What 4 things make turbulence (a high Re) highly likely?

A

High velocity flow

Large diameter vessels

Low blood viscosity

Abnormal vessel wall

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47
Q

How many times more viscous is static blood compared to flowing blood?

A

100 times

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48
Q

What is the principle behind the auscultatory measurement of blood pressure?

A

It is artificially generated turbulence using a sphygnomanometer cuff

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49
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 (R) of the vessel

T=PR

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50
Q

What are the 3 practical consequences of LaPlace’s Law?

A

1) Control of blood flow

– Low tension is required to oppose blood pressure in arterioles
– Smooth muscle control of arteriole & precapillary sphincters are the sites of tissue blood flow regulation

2) Capillaries

– Can be extremely thin & still withstand the pressure

– Thin walls are essential for exchange processes

3) Aneurysm

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51
Q

What are the 4 factors which regulate tissue blood flow?

A
  1. ACTIVE & REACTIVE HYPEREMIA: Local factors associated with metabolic activity of tissues
  2. FLOW AUTOREGULATION:

In response to changes in arterial pressure - Arterialpressure↑ => arterioles constrict to reduce flow - Arterialpressure↓ => arterioles dilate to increase flow Myogenic response - Stretch-activated Ca2+ channels

  1. VASOMOTION: Spontaneous oscillating contraction of blood vessels
  2. RESPONSE TO INJURY: E.g. endothelin-1 released from endothelial cells - Potent vasoconstriction
52
Q

What is (i) active hyperaemia (ii) reactive hyperaemia?

A

(i) if the tissue is highly active then the rate of blood flow will increase. E.g. by up to 20x in skeletal muscle
(ii) When blood supply is blocked (few s to hrs), blood flow then increases to 4-7x that of normal flow

53
Q

For vasoconstriction there is 3 types of constrictors, name the 3 types & give examples for each.

A

NEURAL = sympathetic nerves

HORMONAL = adrenalin, angiotensin II, vasopressin

LOCAL = myogenic response, endothelin-1

54
Q

For vasodilation there is 3 types of dilators, name the 3 types & give examples for each.

A 
NERVOUS = NO - releasing nerves
HORMONAL = adrenaline, atrial - nitriuretic peptide
LOCAL = decreased oxygen, K, CO2, H, adenosine, nitric oxide, bradykinin
55
Q

At rest, how much of the total cardiac output is in the capillaries?

A

About 5%

56
Q

How is local blood flow regulated (i) acutely (ii) long term ?

A

(i) rapid changes within seconds or minutes. Vasodilator theory is widely accepted (“local factors”)
(ii) change in physical size OR number of blood vessels

57
Q

Through which vessel is velocity of blood flow the slowest? Why is this the case?

A

CAPILLARIES
allows time for diffusion & exchange of nutrients & waste

58
Q

Describe capillary diffusion.

A
59
Q

What is the origin, course and distribution of the right and left coronary arteries?

A

RIGHT: arises from R.aortic sinus & passes between R.auricle & PT. It enters the coronary sulcus & gives a SA nodal branch. Gives a (Rt.) marginal branch before turning onto the inferior surface. It usually gives the posterior interventricular branch. It anastomoses with branches of LCA in the coronary sulcus and at the apex.

  • SUPPLIES: Walls of RA and RV, Sinu-atrial and Atrioventricular nodes, Posterior part of interventricular septum (proximal portion of atrioventricular bundle of His), Small areas of the walls of LA and LV

LEFT: Arises from the left aortic sinus between L.auricle & PT & enters the coronary sulcus. It divides into a circumflex branch (which usually gives a L.marginal) & an anterior interventricular branch (Left anterior descending). It anastomoses with branches of RCA in the coronary sulcus posteriorly and at the apex

  • SUPPLIES: Walls of LA, LV, most of the interventricular septum including part of the AV bundle, Anterior Interventricular (LAD) most commonly affected by atherosclerosis.
60
Q

What/where are the coronary sulci/grooves?

A

Between the chambers

  • *Coronary Sulcus or Atrioventricular groove** - seen on both the anterior (Rt. atrium and ventricle) and posterior (Lt. atrium and ventricle) aspects
  • *Interventricular grooves** (anterior and posterior)
61
Q

What happens when either the LCA or the RCA are obstructed?

A

RCA: is referred to as an inferior infarct & is likely to cause arrhythmias

LCA: obstruction of LAD is referred to as anterior infarct; circumflex-lateral infarct

NOTE: Anterior infarcts may cause catastrophic loss of left ventricular function and the ischaemia may also lead to ventricular fibrillation (cardiac arrest)

62
Q

What is CABG?

A

Coronary Artery Bypass Grafting

  • a bypass of the occluded portion of the vessel

Left Internal thoracic or Internal Mammary Artery (LIMA)
Great Saphenous Veins

63
Q

Describe the venous drainage of the heart.

A

The heart is drained mainly by veins that empty into the coronary sinus & partly by small veins that empty into the right atrium.

The coronary sinus, the main vein of the heart, is a wide venous channel that runs from L to R in the posterior part of the coronary sulcus. It receives the great cardiac vein at its left end and the middle & small cardiac veins at its right end. The left posterior ventricular vein & left marginal vein also open into the coronary sinus.

64
Q

Where does the coronary sinus lie? What does it drain into?

A

Lies between LA & LV

Drains into RA

65
Q

Describe the anatomical position of the conducting system of the heart and how it controls heart rate.

A
66
Q

The Autonomic System controls heart rate, force of contraction and therefore, cardiac output via what 2 mechanisms?

A
  1. Sympathetic cardiac nerves from both sympathetic trunks
  2. Parasympathetic cardiac branches from both left and right

vagus nerves

67
Q

Where is the cardiac plexus located? What does it send branches to?

A

Lies inferior to the aortic arch

=> adjacent to the bifurcation of both the PT & the trachea. It sends branches (both afferent and efferent) to the SA node, the AV node, the cardiac musculature and the coronary arteries

68
Q

Describe the nerve supply to the heart.

A

Parasympathetic decreases HR as well as decreasing the calibre of the coronary arteries

Sympathetic increases HR & force of contraction

The vagal afferents detect changes in BP & blood chemistry

The sympathetic afferents return to their site of origin from the spinal cord – T1 to T4

Consequently cardiac pain is referred to the anterior chest wall & possibly medial aspect of the left arm

69
Q

What does MI affect? What can it potentially cause?

A

affects the bundle of His, or the bundle branches

May potentially cause cardiac arrythmias

70
Q

What does the cardiac skeleton separate? What can damage to the blood supply of the conducting system cause?

A

It separates the myocardium of the atria and ventricles, preventing spread of the impulse.

Damage will lead to alterations in rate or order of contraction

71
Q

The first wave of conduction is initiated by the SA node, describe this process & in turn describe the SA node in greater detail (nerve supply, blood supply)

A

The SA node initiates and regulates the impulses for the contractions of the heart, giving off an impulse approximately 70 times per minute in most people most of the time. The contraction signal from the SA node spreads myogenically (through the musculature) of both atria. The SA node is supplied by the sinu-atrial nodal artery, which usually arises as an atrial branch of the RCA (in 60% of people), but it often arises from the LCA (in 40%). The SA node is stimulated by the sympathetic division of the autonomic nervous system to accelerate the heart rate and is inhibited by the parasympathetic division to return to or approach its basal rate.

72
Q

Describe the process of the transfer of signal from SA node to AV nodes.

A

The signal generated by the SA node passes through the walls of the RA, propagated by the cardiac muscle (myogenic conduction), which transmits the signal rapidly from the SA node to the AV node. The AV node then distributes the signal to the ventricles through the AV bundle.

The AV bundle, the only bridge between the atrial & ventricular myocardium, passes from the AV node through the fibrous skeleton of the heart & along the membranous part of the IVS.

73
Q

The atrioventricular (AV) bundle of His should be the only conductive route through the fibrous skeleton, what does it divide to form?

A

Right bundle branch, Left bundle branch, then Purkinje fibres (subendocardial plexus)

NOTE: Impulse is carried to the apex of the ventricles and papillary muscles

74
Q

Describe viruses and their basic biology that makes treatment possible.

A

To replicate they have to attach & enter a living host cell-animal, plant or bacterial-& use its metabolic processes. The binding sites on the virus are polypeptides on the envelope or capsid.

The receptors on the host cell, to which the virus attaches, are normal membrane constituents-receptors for cytokines, neurotransmitters or hormones, ion channels, integral membrane glycoproteins, etc.

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 cell’s machinery for synthesizing nucleic acid & protein & the manufacture of new virus particles.

75
Q

What are the 7 types of antiviral drugs?

A
  1. Viral uncoating: e.g. amantadine/rimantadine
  2. Nucleoside analogue - chain termination e.g. aciclovir
  3. Nucleoside reverse transcriptase inhibitors e.g. lalmivudine
  4. Non-nucleoside reverse transcriptase inhibitors (NNRTIs) - these inhibit reverse trasncriptase directly e.g. nevirapine, efavirenz, delavirdine & etravirine
  5. Protease inhibitors: target the HIV-encoded protease cause significant include atanzanavir, indinavir, lopinavir, ritonavir & saquinavir
  6. Integrase inhibitors e.g. raltegravir & elvitegravir
  7. Neuraminidase inhibitors e.g. oseltamivir
76
Q

What are the uses of aciclovir?

A

For the treatment of herpes simplex virus & varicella zoster virus infections including:

  • genital herpes simplex (treatment & prevention)
  • herpes simplex labialis (cold sores)
  • shingles
  • acute chicken pox in immunocompromised pts
  • herpes simplex encephalitis
  • prevention of herpes viruses in immunocompromised pts (eg people undergoing cancer chemo)

NOTE: oral aciclovir doesnt decrease the risk of pain

77
Q

Give examples of RNA viruses & explain how they are classified.

A

E.g. influenza (flu), Hepatitis C virus (HCV)

  • are classified according to the sense or polarity of their RNA

POSITIVE-sense viral RNA = similar to mRNA & can be immediately translated by the host cell

NEGATIVE-sense viral RNA = complementary to mRNA & must be converted to +ve sense by an RNA polymerase before translation

78
Q

Where does viral replication typically tend to occur?

A

in the host cell cytoplasm

79
Q

Give named examples of retroviruses, what do these viruses contain? What can some RNA retroviruses transform normal cells into?

A

HIV, human T cell Leukemia virus (HTLV)

contains reverse transcriptase (an RNA dependent DNA polymerase) which makes a DNA copy of the viral RNA

This copy is integrated into the genome & is then termed a provirus

  • malignant cells
80
Q

What are examples of approved antiretroviral drugs?

A

Reverse Transcriptase (RT) Inhibitors

  • nucleoside analogs (NRTIs) = abacavir, didanosine, emtricitabine, stavudine, lamivudine, tenofovir, zalcitabine, zidovudine
  • non-nucleoside analogs (NNRTIs) = delaviridine, efavirenz, etravirine, nevirapine

Protease (PR) Inhibitors = amprenavir, atazanavir, darunavir

Entry Inhibitors = maraviroc

Fusion Inhibitors = enfuviritide

Integrase (IN) Inhibitors = raltegravir

81
Q

What is the MoA for NRTIs & NNRTIs?

A

NRTIs - inhibit viral DNA synthesis by acting as a chain terminator by not offering the 3’-hydroxyl function at the (2’deoxy)riboside moiety, which is required for attachment of the incoming nucleotide

NNRTIs - binding induces conformational changes that inhbit the catalytic activity of RT

82
Q

Why are protease inhibitors necessary?

A

Host mRNAs code directly for functional proteins

In HIV, the mRNA is translated into biochemically inert proteins

A virus specific protease then converts them into various functional proteins

Since the protease doesn’t occur in the host, it’s a good selective-toxicity target

E.g. atazanavir, indinavir, iopinavir, ritonavir & saquinavir

83
Q

What 2 (critical) reaction does HIV integrase mediate?

A

Firstly, 3’ end processing of the double-stranded viral DNA ends

& then strand transfer which joins the viral DNA to the host chromosomal DNA forming a functionally integrated provirus.

84
Q

What are 3 integrase inhibitors?

A

raltegravir, elvitegravir & dolutegravir

Raltegravir = use in pts with HIV resistant to other HAART regimens

Elvitegravir = low-molecular weight, highly selective. Shares the core structure of quinolone antibiotics

85
Q

Entry of HIV into a new cell is mediated by what? What does entry require?

A

Mediated by the Env glycoprotein spike a trimer of gp120 & gp41

Entry requires the receptor CD4 plus one oof 2 receptors - CCR5 or CXCR4

86
Q

What are 2 fusion inhibitors? What is their MoA?

A

MARAVIROC = binds to CCR5, preventing an interaction with gp120. Is also referred to as a chemokine receptor antagonist OR a CCR5 inhibitor

ENFUVIRTIDE = binds to gp41 & interferes with its ability to approximate the 2 membranes. Also referred to as a fusion inhibitor

87
Q

What does HAART stand for?

A

highly active antiretroviral therapy

88
Q

What 2 drugs are inhibitors of attachment to or penetration of host cells? Describe their MoA.

A

Amantadine & Rimantadine

At two stages of viral replication within the host cell, a viral membrane protein, M2, functions as an ion channel. The stages are (i) the fusion of viral membrane and endosome membrane and (ii) the later stage of assembly and release of new virions at the host cell surface. Amantadine blocks this ion channel.

Concentrated in lysosomes and increase the pH of the compartment. They interfere with the fusion of lysosomes and endocytosed viral-containing vesicles.

89
Q

What do M2 ion channels function in?

A

virion uncoating following entry by endocytosis
and maturation of the viral envelope proteins during virus assembly and release.

90
Q

What is the purpose of NA (neuraminidase) inhibitors? What are 2 named examples that have been approved for clinical use?

A

Cleaves sialic acid from the cell surface so that newly made viruses are released & able to spread to uninfected cells

They mimic the sialic acid natural substrate by binding to the NA active site, preventing NA function & hence halting virus replication

  1. Zanamivir (relenza) - nasal spray
  2. Oseltamivir (tamiflu) - oral
91
Q

What drugs are used for the treatment of Hepatitis C? (HINT: there’s 4)

A

Ribavirin

Peginterferon alpha

Simeprevir, Ledipasvir & sofosbuvir

Protease inhibitors (telaprevir, boceprevir paritaprevir)

92
Q

Explain, in detail, how blood circulates through the fetal heart.

A

RA - RV - PA to lungs - Pulm Veins to LA - LV - Aorta & major arteries to all systems - major veins to IVC

The separate pulmonary & systemic circulations involve 2 passages through the heart

  • RIGHT (deoxy) to pulmonary circulation, then back to:
  • LEFT (oxy) to systemic circulation

Extensive hepatic blood supply (liver involved in many aspects of metabolism)

93
Q

Explain in general terms the circulation of blood in the foetus and placenta

A
  • Blood is carried from the foetus in 2 umbilical arteries (branches of the int iliac arteries) to the placenta via the umbilical cord
  • In the placena, blood is oxygenated & picks up nutrients from the maternal blood, across the maternal membrane
  • 1 umbilical vein passes in the umbilical cord back to the foetus & will carry richly oxygenated & nutrient rich blood to the R side of the foetal heart
  • no pulmonary circulation, restricted hepatic circulation. Foetal circulation is modified by 3 shunts or by-passes to avoid the lungs & the liver, but still deliver a richly oxy supply to heart & brain
94
Q

How is the pulmonary circulation by-passed by the foramen ovale?

A

Via the foramen ovale

  • Blood from the IVC enters the RA & most of the blood is directed by a ‘valve’ through an opening in the interatrial wall (septum) = foramen ovale.

IVC - RA - foramen ovale - LA - LV - aorta & systemic circulation

this shunt by-passes the RV & pulmonary trunk

95
Q

Is pressure in the LA high or low? Explain why.

A

LOW

as there is a very restricted pulmonary circulation

96
Q

How is the pulmonary circulation by-pased by the ductus arteriosus?

A

SVC - RA - RV - PT - DA & thoracic Ao

  • 90% of blood by-passes the pulmonary circulation via the ductus arteriosus, which connects the pulmonary trunk to the inferior aspect of the arch of aorta
  • 10% of RV blood passes to the pulmonary circulation where it gives O2 to the developing lungs
  • DA carries venous blood directly into the aorta after the aortic arch & the origin of its branches that go to the head & brain

NOTE: patency of the DA is dependent upon prostaglandins

97
Q

How is the hepatic circulation by-passed?

A

By the Ductus Venosus

50% of blood in umbilical vein by-passes liver via DV

  • the DV empties into the IVC to the RA
  • the IVC is also carrying venous blood back from the lower part o the body of the foetus, as well as the reduced hepatic circualtion

=> after the DV joins it, the IVC contains a mix of oxy & deoxy blood

  • the blood in the IVC is still the most richly oxygenated blood available to foetal tissues & it passes from the RA directly to the systemic circulation via the foramen ovale
98
Q

What 3 major events happen at birth?

A
  1. The pulmonary circulation is established immediately
  2. Obliteration of the ductus arteriosus, in 2 phases
  3. Obliteration of the ductus venosus
99
Q

Describe how the pulmonary circulation is established at birth.

A

The first breath pulls blood into the pulmonary circualtion

  • blood from pulmonary circulation is returned to LA
  • pressure rises in LA & equalises with RA
  • foramen ovale CLOSES
  • fossa ovalis visible on the interatrial septum in RA of post natal heart

Patent foramen ovale (PFO) = consequence of non-closure. Tends to be asymptomatic but may cause paradoxical emboli.

100
Q

What are the 2 phases which obliterate the ductus arteriosus?

A
  1. Initial phase during the first hour due to smooth muscle constriction:
    - oxygen is a potent constrictor of the DA & the O2 tension of blood in the Ao & PT increases after the first breath. The mechanism becomes more powerful closer to full term (premature babies at risk of patent DA)
    - levels of PGs fall as they’re no longer produced by the placenta & are removed from the circulation by the functioning lungs. Fall in PGs leads to DA closure

NOTE: drugs that inhibit PG synthesis may be given to promote closure

  1. Later, anatomic closure results from thickening of the tunica intima that occurs over a period of between 1 & 3 months
    - the postnatal remnant = ligamentum arteriosum (between PT & Ao arch)
101
Q

What risks are associated with a patent ductus arteriosus?

A

Postnatally, the aortic pressure is greater than in the PT

Blood will flow back into the pulmonary circulation

  • possibly causing pulmonary hypertension & congestuve cardiac failure
102
Q

How is the ductus venosus obliterated?

A

With the delivery of the placenta, the umbilical vessels contract & undergo obliteration over a period of days

  • the postnatal pattern of the hepatic circulation becomes established & the ductus venosus becomes the ligamentum venosum
  • the umbilical vein becomes the ligamentum teres
103
Q

When a baby is born and takes its first breath, the change in pulmonary pressure and rise in O2 causes which embryonic vessel to constrict?

A

Ductus Arteriosus

104
Q

The foetal circulation differs from the post natal circulation. Through which vessel does oxygenated blood travel from the placenta to the foetus?

A

Umbilical vein

105
Q

Where does the heart tube form?

A

In the mesoderm from angiogenetic clusters, as a horseshoe at the cephalic end of the trilaminar disc

106
Q

What is the first system to develop in the embryo? By what day is there heart development?

A

The vascular system

By day 18

107
Q

How does development of the heart begin? In what 2 directions does the trilaminar disc fold?

A

Begins as angiogenetic clusters that coalesce to form a horseshoe in the mesoderm, as a result of folding of the disc the 2 limbs of the horseshoe fuse to form a single heart tube that lies in the thorax & initially consists of endothelial cells only

  • cephalo-caudal & lateral folding (starts about day 18)
108
Q

Describe the early development of the heart tube.

A

Head & tail folds meet at 2 lateral folds at umbilicus. The lateral foldign swings the 2 limbs of the horseshoe so that they fuse as a single heart tube.

Cephalo-caudal folding casues the heart tube to effectuvely migrate from the head end of embryo, throguh the neck & in to the thorax.

It elongates & develops epicardium (visceral pericardium), myocardium (cardiac muscle) & endocardium (endothelial lining)

109
Q

What is dextrocardia?

A

If the ‘ends’ fold to the left, the developing heart is pushed to the right

110
Q

The atrium bulges out on each side of the bulbus cordis. What will the (i) proximal (ii) middle (iii) distal part form?

A

(i) RV
(ii) the outflow of the ventricles
(iii) PT & Aorta

111
Q

What is between the atrium & ventricle?

A

A narrowing = the atrioventricular canal

112
Q

Endocardial cushions are derived from neural crest cells. Enlargement of these masses forms what?

A

Interatrial septum

The membranous part of the IV septum

AV valves (tricuspid & mitral)

Formation of the PT & Aorta from the truncus arteriosus

113
Q

How are endocardial cushions formed?

A

The tissue in the narrowing between the single atrium & single ventricle swells to form the endocardial cushions

these grow to meet in the middle & divide the AV canal into right (tricuspid) & left (mitral) channels

114
Q

Describe, in detail, the formation of the interatrial septum.

A

The septum primum grows down towards the endocardial, AV cushions. Blood passes from RA to LA via the foramen (ostium) primum

Before the foramen primum closes, perforations appear in the upper part of the septum & develop into the foramen (ostium) secundum

Septum secundum (stiff, muscular & to the right of S.Primum) grows down, but does not fuse with Endocardial Cushion & forms foramen ovale

Blood passes from RA to LA through 2 openings: foramen ovale & foramen secundum

115
Q

During what weeks is the interatrial formed?

A

Weeks 5 and 6

116
Q

What is an Atrial Septal Defect?

A

More common in female infants

Patent Foramen Ovale may be asymptomatic

Foramen secundum defect OR Foramen primum

SOMETIMES, the interatrial septum is totally absent

117
Q

What are the 4 elements of the formation of the IV septum that make defects more possible?

A

Endocardial cushions form left & right ridges in the conus

An extension of the inferior atrio-ventricular cushion will contribute to the membranous portion of the IV septum

Proliferation of, & ventricular growth around, forms the muscular portion of the IVS

The left & right truncal ridges spiral & fuse to form the conotruncal septum

The ridges (i.e. septum) advance inferiorly towards the muscular IVS, making the temporary interventricular foramen smaller & smaller; ventricular growth makes the muscular septum effectively advance towards the truncal septum too

118
Q

What is the interventricular foramen closed by? What is this derived from?

A

By the membranous part of the interventricular septum, derived from the truncal ridges & the inferior atrio-ventricular cushion

119
Q

What are the types of Ventriculo-septal Defects? Who are they most common in?

A

No truncal ridges, no spiral to the ridges

FALLOT’S TETRALOGY = truncal septum deviates right & does not meet the interventricular septum

More come in males

120
Q

Describe atrial growth & ventricular growth.

A

The atria grow, but also need to incorporate the adjacent veins (sinus venosus).

In the right atrium, the crista terminalis marks the change and the original atrium shows muscular ridges (musculi pectinati) while the atrium derived from foetal vein (sinus venosus) is smooth

The two ventricles “balloon” to grow around and away from the muscular septum dividing them

121
Q

What are the pulmonary & aortic valves formed from?

A

Hollowing of endocardial tubules

122
Q

Describe arterial development.

A

It is intimately associated with the sequential formation of the paryngeal or gill arches that have their own cranial nerve & arterial supplies

The arches give rise to sructures in the head & neck

As each pharyngeal arch develops an artery arises from the aortic sac ( the part of the truncus arteriosus that will become the Ao), grows through the gill arch & joins the dorsal aorta

123
Q

What do each of the following form (i) 1st arch (ii) 3rd arch (iii) left 4th arch (iv) right 4th arch (v) Left 6th (vi) Right 6th arch?

A

(i) maxillary arteries
(ii) common carotid arteries
(iii) aortic arch
(iv) right subclavian artery
(v) pulmonary trunk & ductus arteriosus
(vi) pulmonary trunk

124
Q

Explain what is meant by a patent ductus arteriosus.

A

Postnatally the aortic pressure is greater than than the pulmonary trunk

Blood will flow back intot he pulmonary circulation

125
Q

What is coarctation of Aorta?

A

Aortic narrowing after the origin of the left subclavian due to an abnormality in the aortic media & intimal proliferation

May be proximal or distal to the ductus arteriosus

Postductal is more common & blood travels in the subclavian to internal thoracic to intercostal vessels & back to the thoracic aorta - femoral pulses will be weak

126
Q

Where do the Recurrent Laryngeal Nerves originate from? What is their path? What happens on the Right & Left?

A

Branch from the vagus nerves & hook around the 6th arch , before “recurring” up to the larynx

On the left, the arch persists as the ductus & ligamentum arteriosus(um), so the RLN is carried in the thorax

On the right, the 5th & 6th arches regress & the RLN hooks around the 4th arch (passing inferior), i.e. the subclavian artery at the root of the neck NOT in the thorax

127
Q

The foetal circulation differs from the post natal circulation. Which embryonic structure is NOT correctly matched with its postnatal derivative?
a. umbilical artery - medial umbilical ligament

b. ductus venosus - ligamentum venosum c. ductus arteriosus - ligamentum teres
d. foramen ovale - fossa ovalis
e. sinus venosus – right atrium

A

c. ductus arteriosus - ligamentum teres

MD3001 (14 decks)

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