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UofG Medicine Question Bank 2020 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

How are the AV valves attached to the heart?

A

Chordae tendinea attach valves to the papillary muscle

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2
Q

How do semilunar valves close?

A

Pressure gradient caused by blood being pushed back following contraction

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3
Q

Describe the steps of the cardiac cycle?

A

Atrial Systole begins
Atrial Systole ends, atrial diastole begins
Ventricular systole first phase (AV valves pushed closed by ventricular contraction- contraction not strong enough to open semilunar though)
(Isovolumetric contraction)
Ventricular systole second phase (pressure of ventricle exceeds arteries, causing semilunar valves open -> blood ejected)
Ventricular diastole early (Ventricles begin to relax, ventricular pressure drops, semilunar valves close due to backflow)
(Isovolumetric relaxation)
Ventricular diastole late (all chambers relaxed, ventricles fill passively)

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4
Q

When does isovolumetric relaxation and contraction occur?

A

Contraction- between atrial systole ending/ diastole beginning and ventricular systole first phase starting
Relaxation- at the start of ventricular diastole

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5
Q

When do the valves open and close?

A

Semilunars open- when ventricular pressure exceeds aortic pressure
Semilunars close- when aortic pressure exceeds ventricular pressure
AV valves open- when ventricular pressure has dropped and is equivalent to atrial pressure
AV valves close- when ventricles begin contraction

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6
Q

What is inotropy and how does positive/negative inotropy impact stroke volume?

A

Contractile capability of the heart itself- how contractile the cells are
Positive- greater response of contraction (would increase stroke volume)

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7
Q

What is the equation for cardiac output?

A

Stroke volume x Heart Rate

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8
Q

What is the equation for blood pressure?

A

Cardiac Output x Peripheral Vascular Resistance

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9
Q

What do cardiac contractile units look like?

A

Arranged linearly using intercalated discs
Contain a lot of mitochondria
Arranged in parallel with each other to enhance contraction efficiency

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10
Q

What is the resting membrane potential of cardiac myocyte cells?

A

Around -80mV

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11
Q

What is the general concentration of K, Ca and Na in cardiac cells?

A

High K intracellular concentration

Low intracellular Ca and Na

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12
Q

What is the plateau phase and what causes it

A

Equal flow of ions in and out of cardiac cells

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13
Q

What are the steps of cellular action potential of triggering contraction of cardiac myocyte cells?

A 
Phase 0- Opening of voltage gated Na channels allowing for inward Na current. Rapid depolarization 
Phase 1 (notch)- Activation of outward K causing initial repolarization
Phase 2 (plateau)- Balance of inward Ca and outward K flow- Plateau phase
Phase 3- Repolarization phase, outward K predominates
Phase 4- Resting action potential
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14
Q

Do SA node cells ever reach resting membrane potential?

A

No, always active

Similar in AV node

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15
Q

What is the back-up mechanism set up by the cells in the heart?

A

SA Node has constant slow depolarization with spontaneous depolarization.
AV node has this too but it is spontaneously active at a lower rate (intrinsically active in case something happens to the SA node)
Pirkinjes do this too

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16
Q

How does calcium levels relate to action potential and contraction of the heart?

A

Action Potential depolarization causes increase in intracellular calcium transient, this allows for calcium binding to troponin, and binding of myosin to actin causing contraction

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17
Q

Describe the movement of Calcium during the Ca induced Ca release.

A

L type calcium channels open (due to depolarization), allowing more calcium influx from T-tubule.
Ca reaches sarcoplasmic reticulum. Ryanodine Receptor on SR sense incoming of calcium through L-type calcium channel following action potential, and will then allow calcium release from SR.

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18
Q

What is the L-type calcium channel?

A

Voltage gated calcium channel that allows inward flow of calcium once action potential initiates its opening

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19
Q

What causes relaxation of cardiac cells (related to calcium) following contraction?

A

Pump on SR pumps calcium into SR to store
Calcium exchanger moves calcium out of cells
Lack of intracellular calcium causes blocking of actin from myosin via troponin re-binding

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20
Q

What exchanger(s) moves calcium out of cardiac cells?

A

Ca-Na exchanger: Moves 3 Na into cell in exchange for 1 Ca out
ATP pumps: Used to move Ca out.
K-Na Pump: used to exchange 3 intracellular Na out, for 2 K, helping to control ion levels

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21
Q

Where do the coronary arteries stem from?

A

Aortic sinus

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22
Q

When does coronary flow occur?

A

During ventricular diastole
Aortic Valve shuts, pressure in ventricle falls, there is now a pressure gradient- higher pressure in aorta, and lower in ventricular muscle allowing for coronary flow (blood will flow backwards in aorta due to the higher aortic pressure and blood will flow down to coronary arteries)

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23
Q

What structure makes up the inferior, superior, right, and left border of the heart?

A

Inferior-Right ventricle
Right- right atrium
Left- Left ventricular wall
Superior- great vessels, part of left and right atrium

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24
Q

What is occurring within the heart between the lub-dub?

A

Ventricular systole is beginning and ending during this period
Ventricular pressure is high, aortic pressure is high

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25
Q

What do the lub-dub noises during auscultation represent?

A

Lub- Closure of AV valves

Dub- Closure of semilunar valves

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26
Q

When does the radial pulse occur while auscultation?

A

During the 1st and 2nd lub-dub

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27
Q

Where would you listen for the aortic valve?

A

2nd-3rd right intercostal space

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28
Q

Where would you listen for the pulmonic valve?

A

2nd-3rd left intercostal space, adjacent to the sternum

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29
Q

Where would you listen for the mitral valve?

A

Midclavicular line at the 4-5th intercostal space on left side.

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30
Q

Where would you listen for the tricuspid valve?

A

Left sternal border towards the apical level of the heart (4th 5th intercostal space)

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31
Q

What does Jugular Venous Pressure determine?

A

Atrial pressure

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32
Q

What cardiac diseases impact the mechanics of the heart?

A

Cardiomyopathy

Valvular Disease

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33
Q

What cardiac diseases impact the electricity of the heart?

A

Arrhythmias

Conduction System Disease

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34
Q

What cardiac diseases impact the blood supply of the heart?

A

Coronary Heart Disease

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35
Q

When examining a patient for cardiovascular check-ups, what can be observed in the hand/feet and what could this indicate?

A

Nail Beds: Splinter Haemorrhages (infective endocarditis)
Osler nodes: Found typically on toes and fingers (subacute endocarditis)
Janeway Lesions: Red, painless lesions on palms/soles caused by septic microemboli (could indicate acute endocarditis)
Peripheral Cyanosis: COPD, heart failure, abnormal haemoglobin, local vasoconstriction (cold environment)
Clubbing: Loss of nail bed angle (lung cancer, pulmonary fibrosis, atrial myxoma (non-cancerous tumour), congenital cyanotic heart disease)
Tendon Xanthomas: subcutaneous nodules (hyperlipidaemia/cholesterolemia)
Pallor: anaemia, low cardiac output states, peripheral vasoconstriction during shock

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36
Q

What are signs of endocarditis?

A

Splinter Haemorrhages
Osler nodes
Janeway Lesions

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37
Q

When checking radial pulse, what are you looking for, and what can variations of these indicate?

A

Rate
Rhythm: regular, regularly irregular (i.e. regular dropped beat in 2nd degree blockage), irregularly irregular (atrial fibrillation, ectopic beats)
Volume: weak (shock), strong (anaemia, fever, hyperthyroidism)
Character: Regular rise with quick collapse (aortic regurgitation), slow to rise (aortic stenosis)

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38
Q

When examining the heart, what can evaluation of the eyes indicate?

A

Conjunctival Pallor: Anaemia
Xanthelasma: Hypercholesterolemia (cholesterol deposit under skin around the eyes - typically congenital)
Corneal Arcus: Hypercholesterolemia / hypertriglyceridemia (milky-blue deposit around cornea)

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39
Q

When examining the heart, what can evaluation of the mouth indicate?

A

High arches palate: May indicate Marfan’s Syndrome
Central cyanosis: blue-ish tongue/ mucous membranes due to hypoxaemia (pulmonary embolism, congenital cyanotic heart disease)

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40
Q

What can a visual presence of jugular ventricular pressure pulse indicate, and how does it look??

A

Can indicate heart failure, valvular disease (tricuspid regurgitation (often have very noticeable pulse), heart block (see cannon waves)
Double pulsation, not palpable, changes with respiration/position changes, pulse can be stopped with pressure

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41
Q

What waves are observed when examining a visible JVP pulse?

A

A and V

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42
Q

Where is the JVP pulsation observed (if visible)?

A

Between two head of sternocleidomastoid, immediately superior to clavicle

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43
Q

What is phenylephrine and what does it do?

A

Agonist of alpha 1 receptors on vessels driving vasoconstriction
This is used as a nasal decongestant (as constriction to nasal cavity reduces congestion)

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44
Q

What role does oestrogen play in vessel constriction?

A

It is a vasodilator and hypotensive.

This relates to why female BP rises following menopause

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45
Q

Do systolic pressure differ in men and women?

A

Yes, women’s are lower up until about 65 when it slowly overtakes men

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46
Q

What is normal structure of a vessel and what is found in each layer? Start most superficial.

A

Perivascular fat
Tunica adventitia- nerves, macrophages, fibroblasts , stem cells, elastin, collagen.
Media- smooth muscle cells
Intima- Endothelial cells

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47
Q

How do endothelial cells within the tunica intima communicate with smooth muscles cells within the tunica media?

A

Via small whole in the internal elastic lamina
This layer separates the intima and media
The wholes can shrink with hypertension

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48
Q

What happens to vessel walls with hypertension and why?

A

Vessel increases in length because smooth muscle cells are arranged in helical fashion, perpendicular to axis of flow (like spring)
Vascular remodelling– increased lumen to media ratio, media gets thicker, lumen gets thinner (this increases resistance)

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49
Q

What impacts flow the most, radius or length?

A

Radius have largest impact on flow

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50
Q

What is inward and outward vessel remodelling?

A

Inward- narrowing of vessel lumen

Outward- widening of vessel

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51
Q

How can vessel wall change in terms of thickness?

A

Hypertrophic- vessel gets thicker
Eutrophic- no change in vessel thickness
Hypotrophic- thinning of vessel wall

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52
Q

Why is patient compliance so important in terms of hypertension?

A

Drugs will reduce pressure for patients, and they will start to feel normal and not want to continue meds.
However, vessels have undergone remodelling and will go back to hypertensive state.

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53
Q

What role does angiotensin 2 play in terms of tunica media?

A

Vasoconstrictor
Increased in those with hypertension
Growth factor that causes muscle cells to proliferate and migrate

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54
Q

What drugs are best in terms of reversing remodelling changes caused by hypertension?

A

ACE inhibitors like perindopril

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55
Q

Why does remodelling of vessels occur due to hypertension?

A

When you have high BP your vessels remodel to accommodate the increased pressure and protect downstream organs

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56
Q

What do sympathetic nerves release from their axons and what does it act on?

A

Noradrenaline neurotransmitter acts on alpha and beta receptors

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57
Q

What is a baroreceptor and where are they?

A

Found at carotid sinus and aortic arch

They are sensors that detect stretch in vessels and signal to brain the amount of pressure present in the vessel

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58
Q

How can you reduce blood pressure using the sympathetic nervous system?

A

Reduce heart rate

Reduce resistance via vascular tone using reduced sympathetic input/drive

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59
Q

Where do the majority of nerves act within vessels?

A

Tunica adventitia border with media

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60
Q

What neurotransmitters act on smooth muscle cells of vessels, and what are their receptors?

A

Noradrenaline- alpha 1 adrenergic (GCPR)
Neuropeptide Y- Y receptors
ATP- Purinergic Receptor- P2x (ligand-gated ion channel)
Called sympathetic triad

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61
Q

What is the name for the lattice network innervating the smooth muscle cells of vessels?

A 
Sympathetic triad (NA, NPY, ATP neurotransmitters)
-allows for fine regulation of contraction of smooth muscle cells.
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62
Q

What are the nerve-mediated response components to vessel contraction?

A

Purinergic - by ATP neurotransmitter

Adrenergic- Noradrenaline

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63
Q

How can you boost contraction in a vessel in relation to the sympathetic triad?

A

A little release of neuropeptide Y will boos the action of ATP and Noradrenaline neurotransmitters on the vessel smooth muscle cells.

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64
Q

How does neuropeptide uptake occur within varicosities?

A

The uptake of neuropeptides is determined by the neuron/recipient at that given synaptic bouton.
Peptide will cycle round the varicosities

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65
Q

How does noradrenaline release and uptake occur?

A

Dopamine is taken up into vesicle where dopamine beta hydroxylase converts it to noradrenaline.
NA is released by vesicle and will stimulate a1 receptors of recipient nerve/cell.
NA also binds a2 receptors on the axon releasing it, causing negative feedback loop (pre-junctional autoinhibition)

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66
Q

What is the U1 uptake mechanism and what is its purpose?

A

Uptake 1 regulates concentration on Noradrenaline in synaptic cleft, and will uptake NA back into releasing nerve if there is too much.

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67
Q

Can fat impact contraction of a vessel?

A

Yes, but it is not fully understood how

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68
Q

How do sensory nerves relate to smooth muscle cell innervation in vessels?

A

Perhaps sensory nerves have some transmitters impacting surrounding fat and smooth muscle cells

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69
Q

What happens prior to the P wave of an ECG?

A

Impulse formation in SA node- does not appear on ECG

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70
Q

What happens at the P wave on an ECG?

A

Depolarization of atrial muscle

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71
Q

What happens at the delay point on an ECG?

A

This is priming event to fill the ventricles.

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72
Q

What happens at just prior to the QRS phase on an ECG in terms of action potentials?

A

AV node signal conducts down bundle of his to left and right branches along septum.
Conduction through purkinje fibres, and first deflections of QRS are seen.

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73
Q

What happens at the QRS phase on an ECG?

A

Ventricular depolarization and atrial repolarization

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74
Q

What happens at the ST segment on an ECG?

A

Inward calcium and outward K currents are balanced and produce plateau in action potential, reflected in ECG following QRS phase.

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75
Q

What happens at the T wave on an ECG?

A

Ventricular repolarization

Much slower than QRS

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76
Q

What is an ECG lead?

A

An electrical vector

Its a view point of the heart- not the wires connecting to the patient

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77
Q

What are the types of vector leads seen on ECG Leads?

A

Unipolar- Measure potential variation at a single point
(Augmented Limb Leads (aVR, aVL, aVF), Chest Leads (V1-V6))
Bipolar- Measure potential difference between two points
(limb leads 1 (Right Arm-Left Arm), 2 (RA-LLeg), 3 (LA-LL))

78
Q

What leads allow for an inferior view of the hearts electrical activity?

A

2, 3, aVF

79
Q

What leads allow for an anterior view of the hearts electrical activity?

A

V1, V2, V3, V4

80
Q

What leads allow for an lateral view of the hearts electrical activity?

A

1, aVL, V5, V6

81
Q

How does polarity of signals impact the waveforms?

A

Movement away from an electrode would result in a negative wave, towards creates positive
Movement moving across electrode (i.e. perpendicular to towards/away) would result in a signal curved wave

82
Q

What is the QRS axis, what is normal?

A

Way to quantify overall depolarization of heart and if results from an ECG are normal.
Normal= -30 to +90.

83
Q

What are the first things that should be done when checking an ECG?

A

Ask for clinical context
Check dates and details
Assess technical quality
Identify P/QRS/T waves with rhythm strips (lead 2 or V1)
Using those complexes, measure heart rate, axis, intervals
Then look at morphology
Don’t rely on automatic interpretations

84
Q

How do you determine HR on and ECG?

A

Count large squares between QRS complexes and divide into 300

85
Q

What are normal time frames for the PR Interval, QRS wave and QT interval?

A

PR- <1 large square (<200ms)
QRS- <3 small squares (120ms)
QT- <11 small squares (440ms)

86
Q

How do you determine if there is deviation on the QRS axis?

A

Lead 1 and 2 should be most positive (found by looking at positivity of the QRS waves in these leads and comparing it to any negative polarity).
If they are more negative, or other leads show stronger positivity, the axis is “spun” towards these particular leads. This can help you identify if different areas of the heart are/aren’t being depolarized as they should be.

87
Q

What are normal patterns to keep in mind when evaluating an ECG?

A

P wave is upright for inferior leads (L2, L3, aVF)
ST segment should be flat
T wave has the same polarity as QRS

88
Q

How are P waves described?

A

Positive
Negative (inverted)
Biphapasic

89
Q

What may a non-flat ST segment indicate?

A

Depressed may indicate blood flow during plateau phase typically caused by ischemia

90
Q

How are QRS waves described?

A 
First deflection negative = Q wave
Positive deflection= R wave
Any neg deflection after R = S wave
Any further pos deflection = R'
Capital letter= dominant wave
Small letter= non-dominant wave
91
Q

How are T waves described?

A

Upright
Inverted
Flat
Also concordant (same) or discordant vs QRS

92
Q

How is a JVP measurement taken?

A

Lay patient flat with head 45 degree towards left.
Begin to ascend patient until jugular pulse begins to lessen, then take a measurement from the manubriosternal junction with the ruler held upright.
Take measure of JVPs maximum height, over 4cm is abnormal.

93
Q

Why is coronary flow diastolic?

A

During systole, the heart it too constricted to allow blood through, but when it relaxes the blood can pass

94
Q

In reference to metabolism, what happens in disease when the heart rate is increased?

A

Aerobic respiration switches to anaerobic metabolism which brings on angina

95
Q

What releases ANP and what does it do?

A

Atrial Natriuretic Peptide
Released by posterior muscle of the heart (receptors here sense increases in volume, and create/secret ANP i response)
It dilates arterioles in kidneys
Essentially works in opposite manner to aldosterone by suppressing reabsorption of Na in collecting ducts, aiding in water loss to reduce BP

96
Q

In the cardiac system (heart and vessels) is hypertrophy or hyperplasia more common?

A

Hyperplasia is more common in vessel walls with plaques

The heart tends to lean towards hypertrophy

97
Q

How is cardiac output influenced by the autonomic system?

A

SA node has input from symp and parasymp (vagus nerve- drops heart rate)

98
Q

What are the different grades of blood pressure (including normal)

A 
optimal- <120/80
Normal- <130/85
High normal- 130-139/ 85-89
Grade 1- 140-159/ 90-99
2- 160-179/ 100-109
3- >180 / >110
Isolated systolic:
grade 1- 140-159/ 80
grade 2- >160/ 80
99
Q

What are primary causes of hypertension?

A 
Smoking
Obesity
diet (salt)
exercise (lack)
genetics
100
Q

What is secondary hypertension?

A

Caused by another morbidity (renal hypertension or pheochromocytoma)
Treated by treating cause
Accounts for 10% of hypertension cases

101
Q

What implications does hypertension have?

A 
Atherosclerosis
Stoke
MI  (due to thrombis)
Heart failure
Renal failure
Retinopathy
102
Q

What clinical benefits are seen in treating high BP?

A

40% reduction of stroke
25% reduction in MI
>50% reduction in heart failure

103
Q

How is BP calculated?

A

BP = total peripheral resistance x cardiac output

Cardiac output= heart rate x stroke volume

104
Q

What leads to isolated systolic pressures?

A

Calcification of vessels

105
Q

What effects do beta blockers have?

A

Competitive reversible antagonist
Reduce effects of sympathetic nervous system on heart tone
Reduce renin release from kidneys
Both result in:
Reduced heart rate and stroke volume (on cardiac muscle) ->
Reduced cardiac output
Speeds up relaxation of heart

106
Q

What systems and/or organs can we impact in order to lower BP via drug action (touch on how)?

A

Block sympathetic nervous system (beta 1 and alpha 1)
Kidney (Diuretics)
Hormones (RAAS pathway- ACE and angio receptor blockers)
Vasodilation or peripheral arterioles (Ca channel blockers)

107
Q

What are two examples of beta blockers?

A

Propranolol (beta1/2)
Atenolol (Beta 1 selective)
WHY ARE WE MOVING AWAY FROM BETA BLOCKERS- there’s always a bit of cross-over

108
Q

What are adverse effects of beta blockers?

A

Activating beta 2 receptors in lungs- big problem for asthmatics
Intolerance to exercise (less able to raise heart rate and forced contraction)
Hypoglycaemia (effects on pancreas)
Vivid dreams (particularly hydrophilic drugs)

109
Q

What are examples of alpha blockers?

A

Phentalamine (alpha 1 and 2)

Doxazosin, prazosin (alpa 1)

110
Q

What impact do alpha blockers have on the body?

A

Competitive reversible antagonist
Reduce BP via reduction in sympathetic tone in arterioles
Reduce peripheral resistance

111
Q

Besides inducing peripheral vasodilation, what can alpha receptor blockers also be used for?

A

Alpha 1 blockers are also used in Benign Prostatic Hyperplasia as it blocks alpha receptors of internal sphincter, helping to reduce constriction and allow for urination

112
Q

What are ACE inhibitors?

A

Inhibit angiotensin converting enzyme on vascular endothelial surface
preventing conversion of angiotensin 1-> 2

113
Q

What physiological changes do ACE inhibitors cause?

A

Reduced blood volume (via reduction in aldosterone which increase Na reabsorption)
Reduces formation of vasoconstricting-angiotensin 2 (reduction in peripheral resistance)

114
Q

What are adverse impacts of ACE inhibitors?

A

Sudden fall in BP on first dose

Persistent irritant cough (reduced breakdown bradykinin, which activates sensory nerves in lung tissue)

115
Q

What are adverse impacts of ACE inhibitors?

A

Sudden fall in BP on first dose

Persistent irritant cough (reduced breakdown bradykinin, which activates sensory nerves in lung tissue)

116
Q

What are angiotensin 2 receptors blockers and the main subtypes?

A

Blocks Angiotensin 2 receptors
Two receptors subtypes AT1 and 2
AT1 mediates vasoconstriction, aldosterone synthesis/secretion, vasopressin (ADH) secretion- thus we want to bind/block this receptor to allow for reduced BP
AT2 may play role in causing vasodilation, thus only want to block AT1

117
Q

What are diuretics and an example?

A

Bendroflumethiazide
Lower BP by reducing volume via increased excretion of Na and therefore water
Additional vasodilator action may also reduce peripheral resistance?

118
Q

What is the main side effect of diuretics?

A

Reduced plasma K

Not good as if you lower K too much it can cause problems with the heart (bradycardia)

119
Q

What are calcium channel blockers and an example?

A

Verapamil, diltiazem, nifedipine
Block L-type voltage channels (present in heart and muscles- these channels stay open a long time to allow calcium entry into cardiac and vascular smoother muscle)
Reduced Ca entry into vascular smooth muscle reduced vascular resistance

120
Q

What is the mechanism of action of L-type calcium blockers

A

Open Channel Block:
When channel opens, the drug goes into the channel and blocks the pore, which doesn’t allow calcium through the pore.
Allosteric modulation:
Bind on different part of receptor to change morphology of the receptor, disallowing calcium to move through

121
Q

What are differences in rate limitations of calcium blockers?

A

Some are non-rate limiting:
They dont change the heart rate much, primarily impact vasodilation
Rate-limiting: Act more directly on the hearts conduction pathway, working to slow and reduce conduction (verapramil, dilitazem- they favour hyperpolarized membranes)

122
Q

What are some adverse reactions to L-type calcium blockers?

A

Headache (dilation of cerebral blood vessels)

Constipation (relaxation of gastro smooth muscle)

123
Q

How would prescription of anti-hypertensives be done in people under 55?

A

Step 1: Ace inhibitors or low-cost angiotensin 2 blocker
Step 2: Combine with calcium channel blocker
Step 3: Add thiazide-like diuretic
Step 4: Consider more diuretics and/or expert advice

124
Q

How would prescription of anti-hypertensives be done in people over 55, or a person of African/ Caribbean family origin of any age?

A

Step 1: calcium channel blockers (why? ACE are less effective in people over 55 or of African descent)
Step 2: Combine with Angiotensin 2 blocker or ACE-inhibitor
Step 3: Add thiazide-like diuretic
Step 4: Consider more diuretics and/or expert advice

125
Q

Where do atherosclerotic plaques build?

A

In the tunica intima

fatty streaks begin to appear in coronary arteries 5-10years later than the aortic

126
Q

Is there a relationship between fatty streaks and atherosclerosis?

A

Fatty streaks are the first visible sign of atherosclerotic plaque formation

127
Q

What is vessel remodelling?

A

Changes in size of vessels to allow for changes in lumen due to things like development of atherosclerotic plaques

128
Q

What causes fatty streak formation?

A

Insult to endothelium (smoking, high shear stress, infection, diabetes, high turbulent flow at certain points)
Increased adhesion and transmigration of leukocytes (once into the intima layer beneath endothelial cells create oxidant stress)
Increased permeability to lipids
Generation of cytokines/ oxidant stress
Establishes a focus of inflammation

129
Q

Why is increased oxidative stress in terms of atherosclerotic plaques development a bad thing?

A

Oxidative stress is a normal response to infection, but here it can damage the structures in the vessels via oxidation of proteins, lipids, and DNA, causing cell damage and more recruitment of inflammatory mediators.
Oxidative stress also causes increases in superoxide, which decreases availability of nitric oxide reducing smooth muscle relaxation

130
Q

What is the formation of atherosclerotic lesion?

A

Formation of lipid-laden foam cells (monocytes/macrophages)
Formation of fibrous cap (which locks lipid build up in place preventing embolism)
Release of MMPs by macrophages
Compensatory vessel remodelling

131
Q

What happens in unstable plaques?

A

Plaque/thrombus is more likely to ruptures, (intraplaque haemorrhage can also occur- in well developed plaques can sometimes have their own blood supplies, which increase plaque size),
If rupture occurs, there’s increased likelihood of activation of the clotting cascade, a thrombus will form, and can lead to MI

132
Q

What happens in unstable plaques?

A

If plaque/thrombus ruptures, (intraplaque haemorrhage can also occur- in well developed plaques can sometimes have their own blood supplies, which increase plaque size),
There is activation of the clotting cascade, a thrombus will form, and can lead to MI

133
Q

What are vulnerable plaques?

A

Plaques with thinner fibrous caps, larger lipid cores, abundance of inflammatory cells (increasing oxidative stress which can damage the plaque), paucity of smooth muscle cells (if plaque binds on to it).

134
Q

What is cholesterol essential for?

A

Incorporating into cell membrane
maintaining membrane fluidity/permeability
production of steroids/fat-soluble vitamins

135
Q

How is the liver important in relation to cholesterol?

A

Monitors cholesterol levels,
regulates it through synthesis, absorption, bile excretion,
drugs used to treat hyperlipidaemia target this process in the liver/gut

136
Q

How is cholesterol transported?

A

Formed into complex with:
Lipids (cholesterol esters with hydrophilic head, triglycerides, free fatty-acids)
Apoproteins

137
Q

What are different Lipoproteins?

A

Chylomicrons - carry Triglycerides to liver, muscle, adipose
VLDL- carry newly synthesized TriG from liver to adipose
IDL- intermediate between VLDL and LDL
LDL- major reservoirs for cholesterol, taken up via LDL receptors by endocytosis (to help synthesize membranes)
HDL- absorb cholesterol released by dying cells , acts as reverse transporter to take cholesterol to liver

138
Q

What is the exogenous pathway of cholesterol absorption and movement?

A
  1. Chylomicrons take absorbed lipids
  2. In capillaries, lipoprotein lipase enzyme attacks lipids and lipoproteins to take off 3 fatty acids so they can be stored in adipose
  3. Left with chylomicron remnant which expresses APOE which interacts with remnant receptors and takes chylomicron into the liver
139
Q

What is the endogenous pathway for lipoprotein metabolism?

A

Free fatty acids stored in liver can be formed into VLDL, which circulates and is broken down (lipase) into LDL and IDL
IDL can be acted on by hepatic lipase to form LDL (remaining IDL can be up-taken by liver)
LDL is then transported to muscle, by extrahepatic cells, or scavenger cells, or received by LDL receptors in liver again.

140
Q

What happens in familial hypercholesterolaemia?

A

Cant take LDL back up into the liver,

So LDL can still be produced, but there are low LDL receptors meaning it isn’t taken back up

141
Q

What is a sign of familial hyperchol?

A

Xanthelasma- fatty cholesterol rich deposits around eye
Xanthomas - deposits of cholesterol in skin
Angina
Calf cramps

142
Q

What are statins, and what is their mechanism of action?

A

Inhibit β-Hydroxy β-methylglutaryl-CoA reductase (HMG-CoA Reductase) in liver (this prevents formation of cholesterol precursors)
Competitively inhibit rate-limiting step in cholesterol biosynthesis
Reduce synthesis of LDL by liver, this level will fall in liver and increase LDL receptors in order to take LDL up out of plasma.
Most effective at night as this is when most biosynthesis occurs

143
Q

Are statins effective in people with familial hypercholesterolaemia?

A

In most severe cases, likely not effective, but recessive inheritance it may help

144
Q

What are elastic arteries?

A

Conducting arteries- very thick tunica media rich in elastin sheets separated by collagen fiber and smooth muscle cells. Contain vasa vasorum for blood supply.
Include aorta, pulmonary, common carotid, brachiocephalic, subclavian, and iliac arteries.

145
Q

What are muscular arteries?

A

Distributing arteries- thick tunica media with concentric smooth muscle cell layers. Media is bordered by internal and external elastin layers
Most abundant artery type in body
Elastin aids in regulating flow to tissue/organs

146
Q

How do skeletal muscle metabolites impact vasoconstriction/dilation of arterioles?

A

The following events within smooth muscle of vessels cause arteriole vasodilation

  • Partial pressure of oxygen (PO2) decreases
  • Partial pressure of carbon dioxide (PCO2) increases
  • Production of H+ ions increases (pH decreases)
  • Temperature increases
147
Q

What layers make up the capillary wall?

A

Tunica intima consisting of 1 layer of endothelial cells
No tunica media
thin or absent tunica adventitia

148
Q

How is blood entry into capillaries regulated?

A

Precapillary sphincters and arterioles.

149
Q

At rest, how much of the total blood volume in the systemic circulation is found in the veins?

A

64%

150
Q

What aspect of the nervous system regulates veins, and what implications can its innervation have?

A

Sympathetic nervous system

Stimulation will cause venoconstriction which will aid in returning blood to the heart

151
Q

What layers make up a vein?

A

Thin tunic intima and media
Thick tunica adventitia
May contain valves (venules do not contain valves)

152
Q

What is the vessel diameter of arteries, veins, and capillaries?

A

Arteries: 4-25 mm
Capillaries: 0.5 µm
Veins: 4-30mm

153
Q

Describe the wall composition of arteries, capillaries and veins in terms of fibrous, muscular, and/or elastic.

A

Arteries: Elastic and muscular
Capillaries: Only endothelium
Veins: Muscular and fibrous

154
Q

What causes dizziness when standing up from a seated position, and how is this corrected?

A

Blood pools to lower limbs, reducing return of blood to heart -> decreased stroke volume/ cardiac output -> fall in systolic bp -> baroreceptor reflex -> sympathetic input -> increased heart rate/ contractility

155
Q

What is orthostatic or postural hypotension?

A

Slow cardiovascular response to postural changes due to loss/reduction in peripheral autonomic (sympathetic) function
Decrease of 20mmHg in systolic or 10mmHg diastolic within 3 minutes of standing are classified as orthostatic/ having postural hypotension

156
Q

What do you feel when you feel a pulse?

A

The propagating pressure wave through the artery

157
Q

What is central venous pressure and how is it determined?

A

The pressure within the vena cavae. It provides an estimate of the pressure within the right atrium of the heart.
Measurement of CVP requires an invasive procedure using catheter.

158
Q

What is jugular venous pressure and how is it determined?

A

Alternative (less invasive) way to estimate the Cardiac Venous Pressure.
Measure elevation distance of JVP from sternal angle while patient is at 45 degree angle.

159
Q

What can Central Venous Pressure elevation indicate?

A

Right-sided heart failure

Hypervolemia of blood/ECM

160
Q

What blood vessels are responsible for regulating blood flow?

A

Arterioles

161
Q

Where is the largest drop in pressure seen within circulation?

A

In arteriole by about 55%

Arterioles also provide the largest resistance to flow

162
Q

What are Korotkoff sounds?

A

Sounds generated by turbulent blood flow that we observe while measuring blood pressure with a sphygmomanometer

163
Q

When checking blood pressure, what sounds indicate systolic and diastolic?

A

Systolic- first turbulent (korotkoff) sounds heard as sphygmomanometer pressure slowly declines
Diastolic- Point where muffling is heard (or disappearance of sound)

164
Q

What is cardiac output and how is it calculated?

A

Volume of fluid leaving the heart per minute

Stroke Volume x Heart Rate

165
Q

What is series vs parallel resistance?

A

Series would be artery -> arteriole -> capillary

Parallel would be the combination of vessels and the different routes blood can take

166
Q

How can you calculate mean arterial blood pressure?

A

Cardiac Output X Total Peripheral Resistance

TPR = change is pressure gradient/ flow rate

167
Q

What is Starling’s Law of the Heart?

A

Up to a point, the heart will pump out whatever volume it receives

168
Q

What is the calculation for mean arterial blood pressure and what is the average range?

A

DP + (1/3 X Pulse Pressure)
Normal range is 70-105mmHg
PP= SP-DP

169
Q

What are the primary mechanisms of autoregulation in relation to endothelial, metabolic, and myogenic vessel diameter?

A

Endothelial: the endothelium is able to produce specific vasodilating factors. These are prostacyclin and the gas, nitric oxide (NO).
Metabolic: when blood flow is reduced, the resultant hypoxia causes localized release of vasodilating factors from tissue surrounding blood vessels.
Myogenic: blood vessels that contain smooth muscle are able to alter their diameter in response to stretch or compression of the blood vessel

170
Q

What is compliance in relation to vessels?

A

How much a blood vessel’s volume changes (ΔV) with a given pressure change (ΔP) is the compliance of the vessel (ΔV/ΔP).
I.e. A blood vessel that easily expands at low pressure is said to have a high compliance.

171
Q

What cells within the kidney are responsible for sensing changes in pressure? Describe both and their role related to bp.

A

Juxtaglomerular Cells- Modified smooth muscle cells in walls of kidney arterioles that release renin in response to decreases in local blood pressure, sympathetic stimulation, and prostaglandin E2 (PGE2) secretion by macula densa
Macula Densa Cells- Detect changes in NaCl within distal convoluted tubule, when bp drops, glomerular filtration drops, and NaCl delivery to here is reduced which stimulates MD release of PGE2 triggering renin release from JG cells

172
Q

What role does angiotensin 2 play in relation to the body?

A

Causes:
ADH (produced by hypothalamus) release from posterior pituitary gland
Resets baroreceptor reflex (preventing input the minute bp begins to rise) by acting on hypothalamic receptors
Increases aldosterone release by adrenal glands
Increases peripheral resistance via arteriole vasoconstriction

173
Q

What is Atrial Natriuretic Peptide, what does it do, and what signals its release?

A

ANP reduces blood pressure
Baroreceptor stretch signals its release from atrial cardiac muscles
ANP effects:
Inhibit renin release from kidneys (leading to vasodilation)
Increases glomerular filtration via afferent dilation and efferent constriction,
Inhibits Na reabsorption at collecting ducts (increasing fluid excretion)
Inhibits aldosterone release from adrenal glands (increasing Na excretion)

174
Q

Does short-term regulation of BP involve nerves and hormones?

A

Involves nerves but not hormones

Long-term involves both

175
Q

When evaluating the time taken to act (i.e. minutes vs hours), where do the following fall: ADH, aldosterone, angiotensin 2, ANP, and renin?

A

Minutes: ADH, ANP, renin, angiotensin II
Hours: Aldosterone
Aldosterone is a steroid hormone and initiates transcription of proteins which takes hours, as opposed to the others (all peptides) which bind extracellular and initiate second messengers

176
Q

What is tampenade?

A

Compression of the heart due to excess fluid and/or fibrous pericardium

177
Q

What is a pericardiocentesis?

A

Remove part of fluid within the pericardial sack

178
Q

What impressions aid in identifying the left/right lung?

A

Left: Aortic arch, descending thoracic artery
Right: Superior vena cava and Azygous veins

179
Q

What is stenosis and what can it cause in terms of pathology?

A

Stiffening of the valves.

Can lead to ventricular hypertrophy as it is harder to pump blood

180
Q

How is the superior vena cava formed?

A

Left and right brachiocephalic veins, each have contributions from internal jugular, and subclavian

181
Q

What is the azygous vein and why is this system important?

A

Drains directly into superior vena cava from the posterior thoracic wall and upper abdomen.
Major contribution to collateral circulation in draining thoracic and abdomen regions

182
Q

What structures are found in the right atrium?

A

Openings of coronary sinus, superior and inferior vena cavas
Fossa Ovalis- in growing foetus, foramen ovale connects right and left atrium, this closes and leaves remnant.
Crista terminalis- boundary between the rough (pectinate muscles) and smooth muscle (sinus venarum) in atrium
Sinus venarum also helps forms SA node and coronary sinus

183
Q

What impact can patent foramen ovale have?

A

Small strokes- clot formed in right ventricle and moves directly into systemic circulation
Migraines (due to lack of lung filtration of toxins)

184
Q

Describe foetal circulation from exchange to the heart.

A

Gas exchange occurs at placenta
Oxygenated blood enters circulation through umbilical vein
Blood can either move into the liver, or can move through ductus venosus passage into the inferior vena cava
Vena cava -> right atrium
Right atrium -> foramen ovale -> left atrium
Left atrium -> left ventricle -> systemic circulation
Some blood in right atrium will still move to right ventricle to supply the lungs. This blood returns via pulmonary veins, and will move directly into the aorta via ductus arteriosus.

185
Q

Why is blood oxygenation lower in the foetal descending aorta?

A

The ductus arteriosus conjoins with the aortic arch, returning partially deoxygenated blood from pulmonary circulation (which was used to supply the lungs) into oxygenated aortic blood. This reduces oxygenation from this point down.

186
Q

What are auto-rhythmic cells?

A

Cells that have capacity to excite and cause contraction.

2 groups, SA node and AV node. SA is dominant

187
Q

What structures are found in the right ventricle?

A

Tricuspid valve
Chordae tendineae- attach cusps of tricuspid valve to papillary muscles
Papillary muscles- attachment of chordae tendineae
Pulmonary valve
Trabeculae carneae- muscular ridges in wall

188
Q

What structures are found in the left ventricle?

A 
Mitral valve
Chordae tendineae
Papillary Muscles
Aortic valve
Trabeculae carneae
189
Q

What structures are found in the posterior mediastinum?

A

Oesophagus
Descending thoracic aorta
Azygous veins (and hemi-azygous)
Thoracic duct (between conjoining of left internal jugular and subclavian- Left Venous Angle)

190
Q

Where are bronchopulmonary lymph nodes found in the thorax?

A

Surrounding the principle bronchi

191
Q

What are the chordae tendinae?

A

Cord-like tendons that connect the papillary muscles to the valves

192
Q

Which vein arches over the hilum of the right lung to drain into the superior vena cava?

A

Azygous

UofG Medicine Question Bank 2020 (42 decks)

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