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Sem 2 Year 1 > Cardiac medicine > Flashcards

Cardiac medicine Flashcards

1
Q

What 4 components (of systole and diastole) can the cardiac cycle be split into?

A
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2
Q

What are the repetitive sequence of events that occur with each heart beat?

A
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3
Q

What is higher pressure; right or left ventricle?

A

The left is higher pressure, this is because the pulmonary vascular system is a low pressure system.

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4
Q

What does a pressure vs time graph look like for a heart beat?

A

Semilunar valve= aortic valve

AV valve= mitral valve

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5
Q

What do the different sections of an ECG represent?

A

P spike= atrial depolarisation

QRS peak= L and R ventricular depolarisation

T= ventricular repolarisation

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6
Q

How does atrial blood pressure remain fairly constant when pressure falls in the left ventricle?

A

The elasticity of blood vessels such as aorta.

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7
Q

What is stroke volume?

A

The volume of blood pumped by each ventricle per beat

Around 75ml, but may double with exercise

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8
Q

What is the ejection fraction?

A

It is the % of volume pumped out.

Usually 55-60%, in exercise can be upto 80% and in heart failure can be 20%.

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9
Q

What is cardiac output?

A

It is the volume of blood pumped per minute (by each ventricle)

CO= heart rate x stroke volume

CO= Blood pressure / Peripheral resistance

Uusally 5L/min at rest, exercise can be 25L/min

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10
Q

What two factors does stroke volume depend on?

A

a) contracility; the force of contraction (adrenaline increases this)
b) end diastolic volume; volume of blood in ventricle at the end of diastole

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11
Q

What is the Frank-Starling mechanism?

A

Stroke volume is proportional to diastole filling.

As end diastolic volume (preload) increases, so does stroke volume

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12
Q

What is peripheral resistance?

A

Also known as afterload

Is the resistance to blood flow away from the heart- altered by dilation or constriction of blood vessels.

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13
Q

Why does cardiac output not decrease much when peripheral resistance increases?

A

Stroke volume will decrease, which leads to an increase in end systolic volume. This leads to an increase in the end diastolic volume and subsequently an increase in stroke volume by the Frank-Starling mechanism

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14
Q

What is the excitation pathway during a heart beat?

A

The Sinoatrial node provides a depolarisating signal that radiates across the right atrium and to the left atrium.

The atrial action potention activates the atrioventricular node, and this travels through the bundle of his to the L and R bundle braches to the purkinje fibres which activates the ventricles.

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15
Q

What are the effects of noradrenaline and acetylcholine on the heart rate?

A

Noradrenaline speeds it up, ACh slows it down.

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16
Q

What ions are involved in the pacemaker potential, action potential creation and repolarisation?

A
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17
Q

What do neurogenic and myogenic mean?

A

Skeletal muscle is neurogenic, it needs a nervous impulse to initiate a contraction.

Cardiac muscle is myogenic, the muscle generates action potentials spontaneously.

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18
Q

What are the differences in the action potentials generated by heart and skeletal muscle?

A

Cardiac APs are much longer, and there is differences in the ions involved:

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19
Q

Where is the source of Ca from heart cells?

A
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20
Q

What is the atrioventiruclar node delay?

A

When the electric signal arrives at the atrioventricular node, there is a short delay to ensure blood has been pushed into the ventricles before they contract

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21
Q

Where are the 12 leads of an ECG placed?

A
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22
Q

What is left and right axis deviation in the heart?

A

The QRS axis represents the net overall direction of the heart’s electrical activity.

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23
Q

How can the ‘axis’ of an electrical impulse of a heart be cancelled?

A
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24
Q

What time does one large box on an ECG represent?

A

Therefore one large box corresponds to 0.2 seconds.

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25
Q

What does the PR interval represent?

A

It represents the time taken to conduct through the atrioventricular node and bundle of His.

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26
Q

What are the two types of Tachyarrhythmias?

A
  • Narrow complex tachycardia- fast atrial fibrillation or atrial flutter (saw-tooth pattern)
  • Broad complex tachycardia (QRS duration > 0.12s)
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27
Q

What does a too short and too long PR interval suggest?

A

Too short- signal is bypassing node (Wolff-Parkinson-white syndrome)

Too long- conductive tissue disorder- first degree heart block

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28
Q

What does ST elevation and depression indicate?

A

Elevation= acute infractio

Depression= ischemia or left ventricle strain

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29
Q

What are the ECG signs for left ventricular hypertrophy?

A

An abnormally tall R wave in the V5,6 leads and a deeper S in V1

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30
Q

How do you calculate the PR interval and what is the normal range for a PR interval?

A

0.12-0.20 seconds (3-5 boxes)

Count number of small boxes and times that by 0.04

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31
Q

What is the most common cause of left ventricular hypertrophy?

A

Hypertension

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32
Q

What does the ECG of right bundle branch block look like?

A

There is an initial smaller R wave as LV is polarised

Then s wave as it is depolarised

Then another R wave as the RV is depolarised late through muscle

Causes

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33
Q

What is the usual ventricular contraction?

A

The fibres of the left bundle branch begin conudction and impulses travel across the interventriular septum from left to right

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34
Q

How can you calculate HR from and ECG strip of regular and irregular heart rates?

A

Divide 300 by the number of large squares between R waves for regular

For irregular, the number of QRS complexes x6 (since a rhythm strip is a 10s recording of the heart)

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35
Q

What is bradyarrhythmia and tachyarrhythmia?

A

B= any abnormality of cardiac rhythm resulting in a slow HR < 60 BPM

A= any abormalility of cardiac rhythm resulting in a fast HR > 100 BPM

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36
Q

What is first degree heart block?

A

When there is slow conduction through the AV node

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37
Q

What does the ECG look like for 1st degree heart block?

A

Regular rhythm

PR > .02s and is constant

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38
Q

What are the different tyes of second degree heart block?

A

Mobitz I- the PR interval is not constant, continues to lengthen until a QRS is missing

Mobitz II- PR interval is constant however miss a QRS complex either randomly, every 2 P waves or 3

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39
Q

What is the treatment for first, second and third degree heart block?

A

First- not usually treatment

Second- pacemaker

Third (complete)- pacemaker, isoprenaline

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40
Q

What is isoprenaline?

A

Used for complete heart block

It is a non-selective beta adrenoceptor agonist

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41
Q

What is 3rd degree (complete) heart block?

A

Atria and ventricles beat independant of each other

QRS’s and P’s have their own rhythm

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42
Q

What does the ECG look like for second degree heart block?

A
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43
Q

What is narrow complex and broad complex tachycardia?

A

Narrow QRS complex tachycardia (NCT) represents an umbrella term for any rapid cardiac rhythm greater than 100 beats per minute (bpm) with a QRS duration of less than 120 milliseconds (ms)

Broad is the same but with a QRS duration of greater than 120ms

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44
Q

What are examples of narrow complex tachycardia?

A

Atrial fibrillation

Atrial flutter

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45
Q

What does the ECG for atrial fibrillation look like?

A

There are no visible P-waves and an irregularly irregular QRS complex, separated by small uneven oscillations.

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46
Q

What does the ECG of a patient with atrial flutter look like?

A
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47
Q

What is the Vaughan Williams classification?

A

It is the most established classification of arrhythmic drugs and is based on both their electrophysioloigcal and pharmacological characteristics

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48
Q

What are anti-arrhythmic drugs?

A

They are drugs which supress cardiac arrhythmias

They may supress the cells that depolarise spontaneously or they may extend the refractory period during which excitable cells cannot be depolarised

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49
Q

What are the different classifications of anti-arrhythmic drugs?

A

Class 1a, 1b and 1c

Class 2

Class 3

Class 4

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50
Q

What property do class 1 anti-arrhythmic drugs share?

A

They block the entry of sodium ions through voltage gated sodium channels

It limits the rate of sodium entry during action potentials

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51
Q

What are the 3 subgroups of class 1 antiarrhythmic drugs?

A

Class 1a= moderate Na+ channel blocking activity and significantly lengthen the action potential because they also block K+ channels in phase 4. Rarely used

Class 1b have weak Na+ channel blocking activity but shorten action potentials of myocardial cells. Rarely used for arrhythmias

Class 1c have the strongest Na+ channel blocking activity but no not significantly affect the length of the action potential

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52
Q

What are examples of type 1 antiarrthymic drugs?

A

Type 1 quinidine

Type 2 lidocaine

Type 3 flecainide, propafenone

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53
Q

What are class II anti-arrhythmic drugs?

A

Beta-adrenoceptor antagonists or beta blockers

Beta blockers reduce the rate of spontaneous depolarisation by decreasing the availability of Ca2+ ions.

Examples-atenolol, metoprolol

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54
Q

What are type III anti-arrhythmic drugs?

A

These block K+ channels involved in repolarisation, thus prolonging the cardiac action potential

Causes QT elongation

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55
Q

What are examples of type III anti-arrhythmic drugs?

A

Amiodarone, sotalol

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56
Q

What are type III anti-arrhythmic drugs used to treat?

A

Tachyarrhthymias resulting from increased automaticity (atrial fibrillation, ventricular tachycardia)

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57
Q

What property do type IV anti-arrhythmic drugs share?

A

They block voltage sensitive L-type calcium channels. They slow conduction in the pacemaker cells and the atrioventricular node

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58
Q

On what cells do the different classes of antiarrhythmic drugs act on?

A

Class I= myocardial cells

Class II= pacemaker cells

Class III= myocardial cells

Class IV= pacemaker cells

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59
Q

What anti-arrthymic drugs cannot be classified according to the Vaughan Williams classification system?

A

Digoxin, adenosine and magnesium

Sotalol has both class II and III properties

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60
Q

What is the treatment for bradyarrthymias?

A

Temporary or permement pacemakers

Muscarinic antagonist- atropine

Adrenergic drugs such as adrenaline

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61
Q

What is atrial fibrillation?

A

It involves disorderly atrial depolarisation that is no longer coordinated by the SA node

results from multiple small re-entry circuits, predominantly within the left atrial muscle, that cause it to fibrillate rather than contract.

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62
Q

What is atrial flutter?

A

Involves a rapid circuit of depolarisation around the right atrium, usually close to the tricuspid valve

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63
Q

What is atrial tachycardia?

A

Atrial tachycardia involves the establishment of an ectopic pacemaker in the atria, which ini;ates the depolarisa;on of the cardiac conduc;on system in preference to the sinoatrial node. There may be a single ectopic focus or mul;ple foci.

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64
Q

What is atrialventricular nodal re-entry tachycardia?

A

involves the establishment of a rapid re-entry circuit within the atrioventricular node that becomes the pacemaker that drives rapid ventricular depolarisa;on.

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65
Q

What is atrioventricular re-entry tachycardia?

A

the re-entry circuit involves an aberrant bypass tract that creates an abnormal electrical connection between the atria and ventricles, sometimes called paroxysmal supraventricular tachycardia

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66
Q

What are the 5 common supraventricular tachyarrhythmias?

A
  • Atrial fibrillation
  • Atrial flutter
  • Atrial tachycardia
  • Atrioventricular nodal re-entry tachycardia
  • Atrioventricular re-entry tachycardia
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67
Q

What are the physiological consequences of atrial fibrillation?

A

A rapid iregular heart rate

Reduced ventricular filling

Reduced cardiac output

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68
Q

What is the presentation of a patient with atrial fibrillation?

A

Palpitations

Anginal chest pain

Dizziness or syncope

Can be asymptomatic

Low blood pressure and irregular HR can be seen

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69
Q

What are the treatment goals for patients with atrial fibrillation?

A

Reduce symptoms and prevent complications, especially stroke

Restore sinus rhythm and control rhythm

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70
Q

How can sinus rthym be restored in patients with atrial fibrillation?

A

inus rhythm can be restored by electrical cardioversion, or
pharmacological cardioversion with an oral or intravenous
an;arrhythmic drug (e.g. flecainide acetate, amiodarone
hydrochloride)

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71
Q

What is the difference in treatment pathways between atrial fibrillation that has been present for more than 48 hours and life-threatening newly-onset fibrillation?

A

If atrial fibrillation has been present for more than 48 hours, electrical cardioversion is preferred and should not be agempted until the patient has been fully anticoagulated for at least 3 weeks. If patients present with life-threatening haemodynamic instability caused by new-onset atrial fibrillation, they should undergo emergency electrical cardioversion without delaying to achieve anticoagulation.

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72
Q

What drug is given to maintain sinus rhythm post-cardioversion?

A

Standard beta-blocker e.g. bisoprolol

If this is ineffective, an oral anti-arrhythmic drug

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73
Q

What is the next treatment goal for supraventricular tachyarrythmias if cardioversion is not possible or fails?

A

Controlling ventricular rate- beta blockers or calcium channel blockers or digoxin ( last only effective at controlling rate at rest)

Reduce risk of stroke- anticoagulation with warfarin or apixaban

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74
Q

What beta blockers are used to treat cardiac conditions?

A

Beta-1 antagonists such as atenolol, metoprolol and bisoprolol

This is the predominant receptor type in the heart

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75
Q

Where do beta blockers act in the heart?

A

Beta 1 adrenoceptors..

  • In the SA node
  • In the AV node
  • In the conducting system
  • In the cardiac myocytes
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76
Q

What are beta blockers used for in cardiac conditions?

A
  1. treatment of arrhythmias
  2. treatment of hypertension- reduce CO
  3. treatment of angina pectoris
  4. more recently, heart failure (fix impaired cardiac function)
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77
Q

What are the adverse effects of beta blockers?

A
  • Bronchospasm in lungs
  • lethary due to decreased HR ans blood pressure
  • Cold peripheries
  • May precipitate heart block
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78
Q

What are calcium channel blockers and how do they work?

A

They are a class of drugs that all share the ability to interfere with the entry of calcium ions into excitable tissue via L-type voltage gated calcium channels.

This reduced availability for Ca2+ for participation in action potentials

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79
Q

What are some of the subclasses of calcium channel blockers?

A

Dihydropyridines e.g. amlodipine and nifedipine, act peripherally on arteriolar vessels used for hypertension

Centrally acting drugs e.g. verapamil and dilitazem used for tachyarrythmias

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80
Q

What is the mechanism of action of calcium channel blockers against supraventricular arrythmias?

A

Reduce the rate of membrane depolarisation of SA node

Reduces rate of AV conduction- reducing the ventricular response rate in atrial fibrillation

Does not affect purkinje fibres, the myocytes of the atria and ventricles or bundle of His

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81
Q

What patients should you not give calcium channel blockers to?

A

Those with heart failure

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82
Q

What conditions should you prescribe calcium channel blockers for?

A

Atrial fibrillation and other supraventricular tachyarrhythmias

Hypertension

Angina

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83
Q

How Verapamil administered?

A

It has a relatively short half like and needs to be given 3x a day orally

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84
Q

What are the adverse effects of calcium channel blockers?

A

Vasodilator effects cause hypotension, headache or flushing

Bradycardia or heart failure

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85
Q

What are cardiac glycosides and what is their mechanism of action?

A

Derivived from foxglove plants e.g. digoxin

Digoxin inhibits the sodium/potassium-ATPase pump

by inhibi;ng the Na+/K+-ATPase, digoxin diminishes a factor that drives calcium out of the cell, consequently increasing its availability to bind with troponin and participate in myocyte contraction

Caused increased contractibility

Effect on HR not know- reduced SA firing rate and reduces conduction velocity of electrical impulses through AV node

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86
Q

What are cardiac glycosides used for?

A

Heart failure, not used as much

Atrial fibrillation

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87
Q

How is digoxin administered?

A

Long half life- administered by mouth once daily

If rapid effect needed a loading dose should be given

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88
Q

What are the adverse effects of digoxin?

A

Low therapeutic range

Warning signs of toxicity include anorexia, nausea and vomiting

If taken in too high doses can be pro-arrhythmic

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89
Q

What is atrial flutter?

A

Atrial flutter typically involves a re-entrant circuit of depolarisation in the right atrium around the tricuspid valve annulus.

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90
Q

What does the ECG look like for atrial flutter?

A

A ‘saw-tooth’ pattern with a frequency of around 300/minute. Fortunately, the atrioventricular node cannot conduct at that rate and the ventricles are only activated by every second, third or fourth circuit.

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91
Q

What are the goals of treatment for atrial fibrillation?

A
  • restoration of sinus rythm
  • prevention of recurrent episodes
  • control of ventricular rate
  • prevention of thromboembolic complications
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92
Q

How can sinus rhythm be restored in atrial flutter, and then maintained?

A

Cardioversion and pharmacological therapy

Give anti-arrhythmic drugs to stop recurrent episodes

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93
Q

What is the treatment goal if sinus rhythm cannot be restored?

A

Ventricular rate can be controlled by drugs that block the AV node such as beta blockers and calcium channel blockers

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94
Q

What is paroxysmal supraventricular tachycardia?

A

Describes the tachyarrhythmia that results from a re-entrant circuit through the atrioventricular node. This produces a rapid regular narrow complex tachycardia.

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95
Q

What does the ECG for paroxysmal supraventricular tachycardia look like?

A
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96
Q

What is the presentation of a patient with paroxyssmal supraventricular tachycardia?

A

Palpitations, may be accompanied by dizziness, breathless and chest pain

Pulse rat is rapid (> 150)

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97
Q

What is the treatment strategy for paryoxysmal supraventricular tachycardia?

A

Vagal stimulation manœuvres such as the Valsalva manœuvre or immersing the face in cold water. Carotid sinus masage would work too

If that does work, give intravenous adenosine

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98
Q

What is adenosine?

A

Naturally occuring nucleoside that is formed from the breakdown of adenosine triphosphate (ATP)

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99
Q

What is adenosines mechanism of action?

A

It binds to A1 receptors in SA and VA nodes which are coupled to G proteins

Activation of this pathway opens potassium channels, which hyperpolarises the cell

G protein also decreases cAMP which reduces calcium entry

Also acts on presynaptic sympathetic receptors to inhibit release of noradrenaline

These actions produce a temporary block of conduction through AV node, abolishing the re-entry circuit

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100
Q

Why is sinus arrhythmia not always regular?

A

This is normal, rate changes with respiration. On inspiration the thoracic pressure changes and blood is sucked into the chest. Therefore more needs to be pumped out. It is the opposite for expiration

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101
Q

What are the causes of AV nodal block?

A
  • Sino-atrial disease
  • Coronary heart disease
  • Aortic valve disease
  • Damage during heart surgery
  • Drugs e.g. beta-blockers, digoxin and calcium channel blockers
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102
Q

How do you treat AV nodal block?

A

Remove any triggering cause

Give atropine and isoprenaline treatment

Permanent pacemaker

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103
Q

What is contraction of the heart known as?

A

Systole

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104
Q

What is the average cardiac output?

A

5L of blood per min

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105
Q

What controls the arteriole tone?

A

Sympathetic nervous system

Hormones e.g. angiotensin 2

Local factors such as nitric oxide

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106
Q

What are the two sides to the capillary fluid equilibrium?

A

HYDROSTATIC pressure tends to filtrate water from capillary to interstitial space

ONCOTIC pressure tends to draw water back into the plasma

Normally the pressure gradients are balanced

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107
Q

What is exiting and entering the capillaries at different points?

A
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108
Q

What can disturb the hydrostatic fluid equilibrium?

A

Oedema- when excess salt and water can’t be excreted from the body in the form of urine, and resultantly is retained in the body’s cells.

Causes include malnutrition, liver disease, inflammation, vasodilator drugs or deep vein thrombosis

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109
Q

What measures afferent information about blood pressure and volume?

A

Pressure= arerial baroreceptors

Volume= volume stretch receptors and juxtaglomerular cells

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110
Q

What circulating hormones effect blood pressure and volume?

A

Pressure= angiotensin II, adrenaline and vasopressin

Volume= aldosterone, natriuetic peptides and vasopressin

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111
Q

What is arterial blood pressure and what units is it measured in?

A

The hydrostatic pressure within the arterial system

Measured in millimeters of mercury mmHg

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112
Q

What is the average ABP in young adults?

A

120/80

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113
Q

How do you calculate arterial blood pressure?

A

ABP= CO x SVR

CO= stroke volume x heart rate

SVR= resistance to blood flow

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114
Q

What is heart rate increased and decreased by? (nervous systems)

A

Increase by sympathetic system; noradrenaline of beta-1 adrenoceptors

Decreased by parasympathtic system; acetylcholine on muscarinic receptors

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115
Q

What controls the radius of a blood vessel?

A

Circulating hormomes

Smooth muscle layer which is innervated by post-ganglionic sympathetic nerve endings to cause vasoconstriction

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116
Q

What are atrerial baraceptors and where are they located?

A

They respond to stretch in the vessels by producing action potentials, info travels in different nerves to the vasometer centre.

Located within the carotid sinus- glossopharyngeal nerve (IX) and the aortic arch- vagus nerve (X)

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117
Q

Where do efferent nerve from the vasomotor centre act apon?

A

SYMPATHETIC= Heart- increase HR or contractibility

Blood vessels- constrict or dilate

Adrenal medulla- release catecholamines

Kidney- ateriolar constriction and renin secretion

PARASYMPATHETIC= heart- decrease HR

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118
Q

What are the differnt types of fluid in the body?

A

Blood volume= 4L

Extracellular (interstitial) fluid= 12L

Intracellular fluid= 32L

These are usually in equilibrium with each other

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119
Q

How much fluid is filtered and output a day?

A

Filters 180L a day from which the urine output is 1.5L a day

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120
Q

What cells release renin when there is low delivery of sodium and water to the kidneys?

A

Juxtaglomerular cells

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121
Q

What is the function of angiotensin II?

A

It is a vasoconstrictor

Increases filtration in kidney

constricts other arteriolar beds to increase systemic vascular resistance

Stimulates the release of aldosterone which acts to conserve sodium

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122
Q

What is the macula densa?

A

Area of closely packed specialised cell in the kidneys. They are sensitive to the concentration of sodium cholride

Contains juxtaglomerular cells

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123
Q

What is oncotic pressure?

A

Plasma has a high concentration of albumin and other proteins that create a draw, which leads to absoprption of water

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124
Q

What system helps to return any excess fluid to the circulation?

A

Lympahtic system

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125
Q

What cauees a reduce and increase in plasma oncotic pressure?

A

REDUCTION= malnutition, chornic liver disease

INCREASE= areas of inflammation when capillary walls become porous

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126
Q

What causes an increase in arteriolar or venous hydrostatic pressure?

A

A= vasodilating drugs e.g. calcium channel blocker

V= venous obstruction e.g. deep vein thrombosis

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127
Q

What allows blood pressure to be maintained during a haemorrhage?

A

When the circulation is volume depleted the hydrostatic pressure is lower which pulls fluid from the extracellular space back into the circulation

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128
Q

Why can small changes in arteriolar tone cause large changes in arteriolar resistance?

A

The Poiseuille equasion states resistance is directly related to the length and viscosity of blood but inversely linked to the 4th power of the radius

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129
Q

What is myocardial contractility influenced by?

A

Contractibility increases in response to noradrenaline, released by postganglionic sympathetic nerve endings acting on beta-1 adrenergic receptors

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130
Q

How does the autonomic nervous system affect the radius of the blood vessels?

A

Noradrenaline acts on adrenoceptors and causes vasocontriction

No siginificant parasympathetic innervation

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131
Q

What is vasopressin?

A

Also called antidiuretic hormone, it is released from the posterior pituitary gland when plasma volume is reduced

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132
Q

What is the afferent input for blood pressure regulation?

A

Afferent info derived from arterial baroreceptors.

Located around the carotid sinus and in the aortic arch

They respond to stretch by producing action potentials

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133
Q

What are the sources of afferent information required too control blood volume?

A
  • the juxtagolmerular cells in the kidney sense sodium and water delivery to the distal tube and respond by releasing renin
  • volume also sensed by low pressure stretch receptors in the RA- when reduced leads to activation of sympathetic nervous system
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134
Q

What is the renin-angiotensin system?

A

The primary defence of glomerular filtration rate

Influences blood pressure, blood volume and electrolyte balance

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135
Q

How is angiotensin II formed?

A

When renin enters the circulation it cleaves off the decapeptide angiotensin I from angiotensinogen. Angiotensin I is then shortened to angiotensin II by the angiotensin coverting enzyme (ace)

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136
Q

What actions does angiotensin II have? (in the kidneys)

A

Locally, it constricts the efferent arteriole to favour an increase in glomerular capillary pressure and filtration.

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137
Q

What actions does angiotensin II have systemically?

A
  • It acts on arteriolar resistance vessels to cause vasoconstriction (increasing systemic vascular resistance and blood pressure),
  • It stimulates thirst and the release of the water conserving hormone vasopressin at the posterior pituitary gland
  • It stimulates the release of the sodium-conserving hormone aldosterone from the adrenal cortex
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138
Q

What are the actions of aldersterone?

A

It acts to conserve sodium in the body, often in exchange for loss of potassium and hydrogen ions

Acts mainly on kidneys but also on GI tract

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139
Q

What role does the sympathetic nervous system play when there is low blood volume?

A

Increases rate and contracility of heart

Systemic vascular resistance also increased

Veins also restrict- lose reservoir function

Arteriolar contraction in kidneys- reduces glomerular filtration and urine production

Secretion of renin at juxtoglomerular cells

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140
Q

What two effects does the signal from macula densa cells when there is a decrease in sodium have?

A

First, it decreases resistance to blood flow in the afferent arterioles via vasodilation, which increases glomerular capillary hydrostatic pressure and helps increase glomerular filtration rate toward normal, and

Second, it increases renin release from the juxtaglomerular cells of the afferent and efferent arterioles, which are the major storage sites for the enzyme renin.

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141
Q

What are causes of haemorrhage?

A

Causes are major injury, complications of surgery and GI bleeding, e.g. gastric ulcers

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142
Q

What is the immediate physiological impact of haemorrhage?

A

Decrease in intravascular volume

Leads to decreased venous return, decreased ventricular filling and reduced cardiac output

This reduces blood pressure, which reduces renal perfusion and the hydrostatic pressure

Perfusion given to priority organs

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143
Q

What afferent sensors are activated in haemorrhage?

A

Baroreceptors

Volume stretch receptors

Juxtaglomerular sensors

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144
Q

What are the immediate efferent responses during haemorrhage?

A

Sympathetic nervous system=

  • increase HR and contracibility via beta-1 adrenoceptors
  • Cause widespread vasoconstriction via alpha-1 adrenoceptors
  • Vasoconstriction sacrifices blood flow to less important organs
  • Reservoir function of veins decreased
  • Increases adrenaline in circulation
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145
Q

What are later efferent responses in haemorrhage?

A
  • renin release from kidneys (due to sympathetic system and also because cells sense decreased sodium and water)
  • This promotes activation of angiotensin II- vasocontrictor
  • reduced hydrostatic pressure favours water absorption into the vasculature
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146
Q

What will continuous blood loss lead to?

A

Hypovolaemic shock

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147
Q

What are the symptoms of hypovolaemic shock?

A

Hypotension

Low urine output

Confusion

Tachycardia

Pale skin

Cold peripheries

Sweating

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148
Q

What is the treatment for hypovoleamic shock?

A

Intravenous fluids and bloods should be given

Source of bleeding found and treated

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149
Q

What are the risk factors for atherosclerosis?

A

Age, male sex, genetics, hypertension, cholesterol, diabetes and smoking

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150
Q

What is the difference between a stable atheromatous plaque and an unstable one?

A
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151
Q

What are the consequences of myocardial ischemia caused by atherosclerosis?

A

Causes a reduced cardiac output- activates the sympathetic and renin-angiotensin systems

This causes vasocontriction that increases blood pressure

Eventually patient can no longer support the blood pressure and renal function and accumulates fluid

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152
Q

How are diruretics used to treat CV disease?

A

E.g. furosemide that reduced sodium and water overload

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153
Q

How are ACE inhibitors used to treat CV disease?

A

Antiotension-converting enzyme inhibitors, e.g. ramipril are used to reduce effects of renin-angiotensin system activation

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154
Q

How are nitrate drugs used to treat CV disease?

A

E.g. glyceryl trinitrate- relaxes veins and arteries to reduce the work of the heart

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155
Q

What are diruretics?

A

Drugs that increase the excretion of sodium ions, cholrine ions and water from the renal tubules, thereby increasing urinary flow

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156
Q
A
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157
Q

What 5 groups can diuretic drugs be split into?

A
  • Loop diuretics
  • Potassium-sparing diruretics
  • Osmotic diuretics
  • Carbonic anhydrase inhibitors
  • Thiazide diuretics
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158
Q

What are the two different types of thiazide diuretics and what are some examples?

A

Divided chemically into

  • true thiazides e.g. bendroflumethiazide or hydrochlorothiazide
  • thiazide-like diuretics e.g. indapamide and chlortalidone
159
Q

Where do thiazide diruetics act?

A

Kidney- distal convoluted tubule, responsible for reabsoption of 5-10% of filtered sodium chloride= mild

160
Q

What is the mechanism of action for thiazide diruetics?

A

Inhibits Na+/Cl- co-transporter on the luminal membrane

Also causes loss of K+, H+ and Mg+ ions

161
Q

What are the clinical indictations for prescribing thiazide diruretics?

A

Most common is hypertension

Rarely for heart failure

162
Q

How are thiazide drugs administered?

A

Once daily by mouth

163
Q

What are adverse effects of thiazide diuretics?

A

Electrolyte imbalances

Episodes of gout (due to decreased uric acid excretion)

Urinary frequency, dehydration

164
Q

What are calcium channel blockers?

A

They are a class of drugs that all share the ability to interfere with entry of calcium ions via L-type voltage-gated calcium channels

165
Q

What are two different subgroups of calcium channel blockers and what are examples?

A

Peripherally acting (known as dihydropyridines)= amlodipine and nifedipine

Centrally acting= verapamil and diltiazem

166
Q

What is the mechanism of action of calcium channel blocks in vascular smooth muscle cells?

A

They reduce the availability of calcium ions that are required for contraction. The resulting relaxation causes vasodilitation, reducing resistance and blood pressure

167
Q

What are the clinical indictations for prescribing calcium channel blockers?

A

Hypertension- peripherally acting drugs

Angina and supraventricular tachyarrhythmias= centrally acting

168
Q

How are calcium channel blockers administered?

A

By mouth once daily

Nifedipine and verapamil have a shorter half life to given as modified release

169
Q

What are the adverse effects of calcium channel blockers?

A

Flushing, headaches and hypotension

Oedma

Constipiation

170
Q

What are ACE inhibitors?

A

Share the property of inhibiting the angiotensin-converting enzyme that generates the vasoactive peptide angiotensin II, following activation of the renin-angiotensin system

171
Q

What are examples of ACE inhibitors?

A

Ramipril, lisinopril and perindopril

172
Q

What are the effects of ACE inhibitors?

A

Angiotensin-converting enzyme inhibitors inhibit the generation of angiotensin II and therefore prevent or reverse it’s effects resulting in reduced vasoconstriction, increased sodium and water excretion, ultimately leading to reduced blood pressure and circulating volume.

173
Q

How are ACE inhibitos administered?

A

Once daily by mouth

174
Q

What are the adverse effects of ACE inhibitors?

A

Excessive hypotension- dizziness and falls

Hyperkalaemia (reduced availability of aldosterone)

Renal impairement (because RA system is the defence of glomerular filtration)

175
Q

What does ACE take part in?

A

Concerts angiotensin I into angiotensin II

Degrades bradykinin- relevent in lungs

176
Q

What is the main reason patients are unable to tolerate ACE inhibitors long term?

A

15% of patients experiance a dry cough due to ACE’s role in the kinin-kallikrien system

177
Q

Where do potassium-sparing diruetics act?

A

In the late distal covoluted tubule- only reabsorbs 5% of filitered sodium

Therefore they are weak

178
Q

What are the two types of potassium-sparing diuretics?

A

Aldosterone antagonists e.g. spironolactone

Sodium channel blocking drugs e.g. amiloride

179
Q

How do aldosterone receptor antagonists work?

A

Potassium-sparing diuretics

The hormone aldosterone binds to its receptor and stimulates the formation of the Na+/K+ exchanger. These drugs stop this

180
Q

How do sodium channel blocker drugs work?

A

Inhibit Na+ reabsorption by blocking luminal sodium channels

181
Q

What are the clinical indications for prescribing potassium-sparing diruetics?

A

For conditions where there is increased circulting concentrations of aldosterone causing sodium and water overload.

E.g. chronic heart failure, liver failure and primary hyperaldosteronism

182
Q

How are potassium-sparing diuretics administered?

A

Oral administeration once daily

183
Q

What are the adverse effects of potassium-sparing diuretics?

A

Hyperkalaemia (a potassium level in your blood that’s higher than normal), potentially fatal

184
Q

How are beta-blockers administered?

A

Daily, by mouth

185
Q

What beta-blockers are most commonly used to treat CV disease?

A

Selective beta-1 blockers

E.g. atenolol, metoprolol and bisoprolol

186
Q

What indications are beta-blockers prescribed for (CV)?

A
  • hypertension (not as effective as other drugs)
  • Anti-arrhythmias
  • Angina pectoris (reduce energy requirements and oxygen demands of heart)
  • Heart failure
187
Q

What is pulse pressure?

A

The difference between systolic and diastolic

188
Q

What are the main responses to changes in blood pressure?

A
  • Barorceptors
  • Chemoreceptors
  • CNS ischemia responses
  • Vessels relax under high pressure
  • Renin-angiotensin system
  • Aldosterone
    *
189
Q

What device is used to measure blood pressure?

A

Sphygmomanometer

Manual blood pressure cuffs are also used now

190
Q

What is white coat hypertension?

A

When a patient become hypertensive due to the stress of being at a GP/ hospital

Can increase blood pressure of 20mmHg

191
Q

What are the signs of hypertensive damage?

A

Kidneys- urinalysis shows a raised level of protein

Heart- ECG shows left ventriculr hypertrophy

Eyes- retionpathy

192
Q

What are the 3 different groups with high blood pressure?

A

Grade 1= 140/90 to 160/100, few to many get CV disease

Grade 2= 160/100 to 180/120, all get CV disease

Grade 3= 180/120+ all- very urgent treatment as there is a risk of acute target organ damage

193
Q

What other factors decide what risk groups patients are in?

A
  • Already have CVD
  • With diabetes
  • With chronic kidney disease
  • Age, smoking, lipids (10yr CV disease > 10%)
194
Q

What lifestyle measurements should be changed in patients with hypertension?

A

Weight reduction

Healthier eating

Dietary sodium reduction

Physical activity

Moderation of alcohol consumption

195
Q

What is the drug pathway for treatment of hypertension?

A

DM= diabetes mellitus

196
Q

What is resistant hypertension?

A

When there is no/ little change in a patient’s blood pressure after being on the 3 drugs.

Need specialist referral

Check for secondary causes

197
Q

What are common anti-hypertensive drugs?

A

ACE inhibitors

ANG-II receptor blockers

Calcium channel blocked

Diuretics

Beta blockers

198
Q

What are common angiotensin-II receptor blockers?

A

Losartan, candesartan

199
Q

What are the side effects of angiotensin receptor blockers?

A

Hyperkaleamia

Renal dysfunction

200
Q

When should ACEi and angiotensin receptor blockers be used and not?

A

Used in patients with diabetes

But not in pregnancy

201
Q

When should calcium channel blockers be used and not used?

A

Used in older patients and patients with agina

Not used in patients with heart block or heart failure

202
Q

When should diuretic thiazides be used and not used for hypertensive patients?

A

Used for older patients with heart failure

Not used in patients with gout or low K+

203
Q

What is primary and secondary hypertension?

A

Primary hypertension is where there is no obvious cause

Secondary is where there is cause- usually endocrine, renovascular, renal or pharmacological cause. Only 5% of cases

204
Q

What are the contributing factors for primary hypertension?

A
  • Western diet- high salt, low potassium, high calorie and low fibre
  • Obesity
  • Physical inactivity
  • Alcohol
  • Stress
205
Q

What are some medications that cause secondary hypertension?

A

Oestrogen oral contraceptives

NSAIDs

Steroids

Cociane, alcohol

206
Q

How does renal artery stenosis cause hypertension?

A

The arterys to the kidneys are narrowed, there will be a drop in renal pressure and the renin-angiotension system is activated

207
Q

What are the causes and management of renal artery stenosis?

A

Causes- atherosclerotic stenosis and fibromuscular dysplasia

Management- ACE inhibitors, diuretics and renal stent

208
Q

What are the 3 parts of the nephron in the kidney where drugs work?

A

The collecting duct (red)

Distal convoluted tubule (orange)

Thick ascending loop (yellow)

209
Q

Where does aldosterone act?

A

The collecting duct of the nephron

210
Q

How does aldosterone act in the kidney?

A

It binds to the nuclear hormone receptor cytosolic

This causes an increase in activity of ATPase- sodium ions in lumen are pumped through and reaborbed, and pottasium is swapped to maintain polarity

Can also have H+ ions swapped or Cl- reabsorbed

211
Q

How does the increase in NaCl cause blood pressure to rise?

A

It causes an anti-diuretic hormone to resorb H2O, when water is reaborbed, the blood pressure rises

212
Q

What is the condition called where an individual produces too much aldosterone and what are the causes?

A

Primary aldosteronism

Causes= a tumour producing aldosterone called Conn’s tumour

Bilateral adrenal hyperplasia

213
Q

What are the symptoms of primary aldosterone?

A
  • blood tests- aldosterone is high
  • the aldosterone is resistant to supression
214
Q

What are the signs a patient may have secondary hypertension?

A
  • They are young and there was a rapid onset
  • They have resistant hypertension
  • They are on drugs that can cause hypertension
    *
215
Q

What are the two lipids most important to CV disease and how they are transported around the body?

A

Cholesterol and triglycerides

Lipoproteins transport these chemicals within the circulation

216
Q

What are the different types of lipoprotein?

A
217
Q

Where are lipoproteins created?

A

The epithelium of the small intestine from dietary lipids

The liver from stored lipids

218
Q

What system takes lipoproteins back to the liver from peripheral tissues?

A

Reverse cholesterol transport

219
Q

What is the exogenous lipid pathway?

A

Formation of chylomicrons in the small intestine

These are large and have relatively little cholesterol content. Enter blood stream via thoracic duct.

Lipoprotein lipase (LPL) breaks it down to produce fatty acids and triglyceride which is taken up by muscle/adipose tissue. The remnant is rapidly absorbed by the liver.

220
Q

What will happen to blood if the patient has the genetic disorered lipoprotein lipase deficiency?

A

Causes an abnormal number of microns in the blood- blood should seperate into a red part and a pale opaque part

221
Q

What is the endogenous lipid pathway?

A

Stored cholesterol is packaged into lipoproteins called very low density lipoproteins.

Delivers fatty acids to muscle/adipose tissue.

VLDL can be secreted into the blood stream in the fasted state. After degredation, turn into a short lived lipoprotein which can either be absorped into liver or can become a low density lipoprotein which is packed with cholesterol

222
Q

What is the reverse cholesterol transport system?

A

High density lipoproteins (formed small intestine and liver) can collect free cholesterol from the peripheral tissues via LCAT enzyme

SRB-1 receptor allows HDL to be resorbed into liver. However HDL can also interact with the enzyme CETP and become VLDL

223
Q

What are the proteins that are found on the outer shell of lipoproteins and determine their behaviour?

A

Apolipoproteins

224
Q

What delivers triglycerides to muscle and adipose tissue?

A

Chylomicrons created in the gut post eating

Very low density lipoproteins synthesised in liver, during fasting state

225
Q

In what form does the liver uptake and decrete cholesterol?

A

Secretion via very low density lipoproteins

Uptake via remnants of IDL, LDL, HDL

226
Q

What types of lipoproteins increase and decrease risk of CV disease?

A

Low density lipoproteins increased rates of CV diseawe

High density lipoproteins decreased it

227
Q

How are lipoproteins taken up by arterial walls and what is the most damaging?

A

If not cleared by the liver, lipoproteins with apolipoprotein B can be take uo into arterial walls

LDL’s are the most damaging as they are long lived

Build up can cause fatty streaks

228
Q

What is atherosclerosis?

A

An inflammatory process where monocytes and free radicals migrate to the arterial wall and transform into macrophages which takes up LDL. Macrophages laden with LDL are known as foam cells= makes up fatty streak. Then plaques form.

229
Q

How are atheromatous plaques formed?

A

Smooth muscle cells are stimulated by macrophages responding to the lipoproteins to migrate, proliferate and differentiate

SMC’s differentiate into fibroblasts which produce a fibrous collagen cap

Foam cells undergo necrosis to leave a pool of extracellular cholesterol

230
Q

What conditions can atheromatous plaques cause?

A

Can reduce blood flow= angina

If it ruptures, can cause myocardial infarction or stroke

231
Q

What is an example of a disorder that causes high low density lipoprotein levels?

A

Inherited disorder of familial hypercholesterolaemia

232
Q

How are coronary arteries with blockages unblocked?

A

A cardiologist will insert a wire into the groin up into the heart, using live x-ray images to pinpoint the site of blockage

Artery is then reopened using a tiny balloon, leaving a tube or stent in place

233
Q

What are the different CV risk calculators and what patients should be given prevention treatment?

A

ASSIGN or QRISK3

In Scotland, treat if risk is > 20%

234
Q

What drugs are given to lower a patient’s lipids?

A

Statins- 1st choice

Ezetimibe- used as a adjunct

Fibrates- used as a adjunct

235
Q

How do statins work?

A

Statins work by limiting the rate controlling step of cholesterol synthesis. They starve the cell of cholesterol and stimulate it to take up LDL, thus removing it from circulation.

236
Q

During development, where does haematopoiesis take place?In fo

A

In foetuses the first haemopatic stem cells emerge from the yolk sac

Later haematopoiesis moves to the liver

Shortly before birth, the bone marrow (red)

Occurs in all bone marrow as an infant but as an adult it occurs in the central skeleton and proximal ends of femur

237
Q

What do all blood cells arise from?

A

The multipotential haematopoietic stem cells

238
Q

What is haemstopoiesis?

A

Hematopoiesis is the process by which the body produces blood cells and blood plasma.

239
Q

What are growth factors for haematopoietic cells?

A

Erythropoiesis- regulates RBC production

Thrombopoiesis- controls platelet count

Granulocytes- boost production of neutrophils

240
Q

What is erythropoisesis?

A

Regulates production of RBC

Produced by liver and kidney in response to low oxygen levels

regulated by renal erythropoietin

241
Q

What is erthrocytosis, leucocytosis and thrombocytosis?

A

Too many red, white and platlet cells respectively

242
Q

What is anaemia, leukipenia, thrombocytopenia and pancytopenia?

A

Too little red, white and platelet cells

Pancy= too little of all blood cells

243
Q

What do RBC look like under a stain?

A

Round with a central area of palour due to them being biconcave disks

244
Q

What are the symptoms an anaemia?

A

Lethary, breathlessness, headache, chest pain, dizziness and pallor

245
Q

What can cause iron deficiency?

A

Chronic blood loss through periods or GI bleeding

Diets such as vegetarian and veganism

Malabsorption such as coeliac disease

Increased requirements e.g. growth

246
Q

What will blood cells look like in a anaemic person?

A

Small, less coloured and middle pale area will be greater

247
Q

What is megaloblastic anaemia?

A

efective DNA synthesis during RBC production causing cell growth without division. Cells are much larger. Usually due to B12/folate deficiency.

248
Q

What is haemolytic anaemia?

A

Due to RBC being destroyed in the peripheries. Normally RBC are removed and recycled after 3 months. HA occurs when they are excessively broken down. Will see spherocytes or fragments in blood.

249
Q

What are causes of leukopenia?

A

Infection, inflammation, steroids, prenacy, lymthoma, leukemia or allergy

250
Q

What causes leucopenia?

A
251
Q

What are causes of pancytopenia?

A

Severe infection

Bone marrow failure

Leukaemia

252
Q

What is the precursor of a platelet?

A

The megakaryocyte in the bone marrow

253
Q

What are the 3 distict stages involved in the formation of a platlet rich thrombus?

A
  • platelet adhesion
  • platelet activation/ secretion
  • platelet aggregation
254
Q

What stabilises the the platelet thrombus?

A

The conversion of fibrogen to fibrin by thrombin and polymerisation of fibrin stabilises the platelet, resulting in a platelet-fibrin clot

255
Q

What generates factor Xa?

A

Exposure of subendothelial collagen and the release of tissue factor

256
Q

What are examples of drugs that inhibit platelet function?

A

Aspirin and COX inhibitors

Reversible COX inhibitors e.g. NSAIDs

257
Q

What is the coagulation pathway?

A

A series of pathways of interactions between proteases, zymogens, enzymes that eventually creates fibrin strands to help form a clot

258
Q

What is the factor 2a in the coagulation pathway?

A

Thrombin; helps to create fibrin strands

259
Q

What is the waterfall theory of the coagulation cascade?

A

Contains a intrinsic pathway, common pathway and extrinsic

260
Q

What is wrong with the waterfall theory of coagulation?

A

Fails to reflect haemostasis

(Patients with fXII deficiency do not bleed)

(Patients with FVII deficiency bleed abnormally)

261
Q

What is the main reason patients with haemophilia bleed?

A

They lack factor 8 or 9 in the coagulation pathway, so are unable to maintain the production of thrombin

262
Q

What laboratory measurements can be done to check the clotting system?

A

Prothrombin time= reflects extrinsic and common pathway

Activated partial thromboplastin time= reflects the intrinsic and common pathway

Both measured in seconds

Fibrinogen= reflects functional activity of fibrinogen. Measured in g/L

263
Q

What is Von Willebrand disease and what is the management?

A

Bleeding disorder, lack of Von Willebrand factor which promote platelet adhesion to subendothelium at high shear rates and carrier molecules for FVIII.

Managment- antifibrinolytics

264
Q

What are the 3 factors in Virchow’s triad?

A

Stasis, vascular injury and hypercoagulability

265
Q

What is Virchow’s triad?

A

A triad of factors of which one needs to be present in order for venous thrombosis to form

266
Q

What is the summary of the revised coagulation cascade?

A

Exposure to tissue factor, known as extrinsic tenase, enables the generation of activated factor X or Xa.

X allows the generation of a small burst of thrombin via prothrombinase

Thrombin enables platelets to back activate the intrinsic tenase enzyme complex which creates Xa- alows for ongoing generation of Xa.

Xa ultimately cleaves fibrin peptides fro, fibribinogen to make a stable fibrin clot

267
Q

What prevents over activity of the clotting cascade?

A

Natural inhibitors such as

  • Tissue factor inhibitor
  • Antithrombin
268
Q

What percentage of deep vein thrombosis patients have it recurring?

A

30%

269
Q

What are the risk factors for venous thromboembolism?

A
  • Older age
  • Obesity
  • Varicose veins
  • Previous VTE
  • Family history
  • Cancer
270
Q

What are the symptoms of deep vein thrombosis?

A
  • Usually unilateral
  • Develop pain, swelling, increased temperature and dilitation of superficial veins
    *
271
Q

What are the different ways of diagnosing DVT and what is the gold standard?

A
  • gold standard= contrast venography (x-ray)
  • D-dimer as a negative predictor
  • venous ultrasonography
272
Q

What are the symptoms of pulmonary embolism?

A
  • Collapsing
  • Fainting
  • Crushing chest pain
  • Breathlessness
273
Q

How are pulmonary embolism’s diagnosed?

A

Chest x-ray, ECG and ABG to rule out other causes

CT pulmonary angiogram

D-dimer

274
Q

What are the different types of anticoagulation drugs and what are examples?

A

Parenteral anticoagulation- heparin, low molecular weight heparin or fondaparinux

Direct oral anticoagulation- apixaban and rivaroxaban

275
Q

What was the traditional management of VTE?

A

Warfarin

At start give heparin or LMW heparin until warfarin effect kicks in

276
Q

What are the different direct oral anticoagulants?

A

Riveroxaban, edoxaban and apixaban are factor X inhibitors

Dabigatran- direct thrombin inhibitor

277
Q

Why does Warfarin need to be monitored?

A

Has a narrow therapeutic range.

278
Q

What is thrombophilia?

A

Thrombophilia is a condition that increases your risk of blood clots. There are different causes.

279
Q

What factor does dabigatran inhibit?

A

IIa

280
Q

What factor in the coagulation cascade changes fibrinogen into fibrin?

A

IIa

281
Q

Why does Heparin require monitoring?

A

There is differences in chain length

282
Q

How does Heparin work as an anticoagulant?

A

It binds to antithrombin and potentiates its inhibitory action towards factor Xa and thrombin

283
Q

What are the side effects of heparin?

A

There is a risk of osteoporosis

284
Q

Why is low molecular weight heparin used?

A
  • Reduced risk of osteoporosis
  • No monitoring required
  • nearly 100% bioavailability
285
Q

How does Warfarin work?

A

It competitively inhibits that activates vitamin K in the body

Factors II, VII, IX and X are dependant on Vit K to be synthesised.

286
Q

How is VTE prevented?

A

Compression socks

Low dose anticoagulants

287
Q

What is athermona and athersclerosis?

A

Atheroma= plaques found in arteries

Atherosclerosis= hardening of the artery

288
Q

How do cells get into a lesion on an artery wall?

A

Can pass through the endothelial cells or by the tunica media

289
Q

What are the 3 layers in an arterial wall?

A
290
Q

What layers of atery are effected by atheroma?

A

The tunica intima

Plaque can enter the tunica media

291
Q

What is another way of putting stasis?

A

Abnormal blood flow

292
Q

What is an embolus?

A

A detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin

293
Q

What are forms of emboli?

A

Thrombi (thromboembolism)

Fragments of bone

Droplets of fat

Foreign bodies

294
Q

What type of pulmonary emboli is associated with collapse and sudden death?

A

Emboli that lodge at the bifurcation as a ‘saddle’ embolus

295
Q

What will medium and small, recurrent pulmonary emboli result in?

A

Medium= pulmonary infarction

Small and recurrent= pulmonary hypertension

296
Q

What are systemic emboli?

A

Refers to emboli that travel through the systemic arterial circulation

80% arise from heart althoug also in aortic aneurysms

297
Q

What is infarction?

A

An area of ischaemic necrosis caused by occulsion of arterial supply or venous drainage

298
Q

What are the causes of infarction?

A

Usually thrombosis and thromboebolism

Expansion of atheroma, compression of vessel, vasospasm, twisting of vessels due to rupture

299
Q

What are the two types of infarct?

A

Red (haemorrhagic)- caused by venous occlusion, occurs in loose tissues or tissues with dual circulation (lung). Where one circulation route gets cut off so there is not enough blood supply and the tissue dies but still blood in tissue.

White (anaemic)- arterial occlusions. Occurs in solid organs eg heart, spleen.

300
Q

What occurs in a cerebral infarct?

A

There is tissue destruction present with formation of cystic spaces and liquefactive necrosis (transformation of the tissue into a liquid viscous mass).

Proteolysis (proteins are broken down) also occurs

301
Q

What is the difference between benign and malignant hypertension?

A

Benign- slow changes in vessels and heart with chronic end-organ dysfunction

Malignant- rapid changes in vessels with acute end-organ dysfunction, BP tends to be higher

302
Q

What are the cardiovascular effects of hypertension?

A

The heart develops left ventricular hypertrophy

This is associated with fibrosis and arrythmias

Increases of coronary artery artheroma, ischaemic heart disease and cardiac failure

303
Q

What effects on the kidney does hypertension have?

A

Nephrosclerosis can occur where the individual nephrons (unit of filtration) in the kidney drop out and disappear- related to chronic renal failure

Malignant hypertension can cause acute renal failure

304
Q

What are the effects of hypertension on the brain?

A

Main effect is stroke by infarction or haemorrhage- blood pressure causes a leak in one of the blood vessels in the brain

305
Q

What is ischaemic heart disease?

A

When blood supply to the heart is insufficient for metabolic demands

Usually due to coronary artery disease

306
Q

What are the causes of atheromatous coronary artery disease?

A

Progressive stenosis

Thrombosis

Emboli from inflammed aortic valve

307
Q

What are the different changes in the heart after myocardial infarction?

A
308
Q

What is cardiac failure?

A

Failure of the heart to pump sufficient blood to satisfy metabolic demands. It leads to under perfusion which causes fluid retention and increased blood volume.

309
Q

What are the differences in acute heart failure and chronic heart failure?

A

Acute= rapid onset of symptoms often with a definable cause, e.g. myocardial infarction

Chronic= slow onset of symptoms, associated with ischaemic or valvular heart disease

310
Q

What is orthopnoea?

A

Breathless whilst lying down

311
Q

What are the causes of cardiac failure?

A
  • Pressure overload due to hypertension or valve disease
  • Volume overload due to valve diseaee
  • Intrinsic cardiac disease, e.g. ischaemic heart disease and conducting system disorders
312
Q

How does the elasticity of the arteries change?

A

Near the heart the arteries are elastic in nature, further away they are robust and strong

313
Q

Why can patients with occlusion disease still have good perfusion to tissues?

A

Arteries have many anastomoses

314
Q

What controls the blood flow in and out of capillaries?

A

The precapillary and post-capillary bed spinchters

315
Q

What is the name of an abnormally dilated artery?

A

Aneurysm

316
Q

What is the name of a abnormally narrowed artery?

A

Stenosis

317
Q

What is the name of a blocked artery?

A

Occluded

318
Q

What is the name of a split artery?

A

Dissection

319
Q

What is the name of an oversensitive artery?

A

Vasospasm

320
Q

What is the name of an inflamed artery?

A

Vasculitis

321
Q

What is the formal definition of aneurysm?

A

1.5x the normal diameter

322
Q

What are the causes of aneursyms?

A

Degenerative aneurysms are the most common (wall has lost its strength). Inflammatory, mycotic (infective) and traumatic can also occur.

323
Q

How does aneurysm repair surgery work?

A

It is an open surgery and places a lot of stress on the patient. A clamp is placed beneath the aorta and at the iliac arteries to stop blood flow. The aneurysm area is replaced by a hand made tube graft. A stent graft can also be used and is minimally invasive.

324
Q

What is the main cause of stenosis and what are the symptoms?

A

Main cause= atherosclerosis

Symptoms- tight hard pain in calves on walking a fixed distance- worse uphil but eases rapidly at rest.

325
Q

What are the 6 P’s of acute blocked arteries?

A
  1. Pain
  2. Palor
  3. Perishingly cold
  4. Parasthesia (burning/prickling sensation)
  5. Pulselessness
  6. Paralysis
326
Q

What are the symptoms of chronic blocked arteries?

A

Short distance claudification

Nocturnal pain

Pain at rest

Numbness

Tissue necrosis

Gangrene

327
Q

What is claudification?

A

Claudication is pain in your thigh, calf, or buttocks that happens when you walk.

328
Q

What is the treatment of occluded arteries or tight stenosis?

A

Putting a balloon through the arteries then inflating it, causing the arteries to widen. Often is only a temporary fix as artery loses elasticity and returns to original form. Stents can provide a more permanent relief by holding the artery open. A bypass graft can also be used, where a surface vein is used. If reconstruction is not available to them, amputation may be needed.

329
Q

What is dissection and what is the treatment?

A

Where the intima becomes detached from the media. It creates two channels of flow- true lumen and false lumen. True lumen is smaller of the two.

Need treatment to widen the true lumen and compress the false one. A stent graft can be used.

330
Q

What can happen to the kidneys in descending aortic dissection?

A

If occurs in descending aorta one kidney will be connected to true lumen and one to false lumen.

331
Q

What is the worry with ascending aortic dissection?

A

That the coronary arteries are involved- immediate surgery is needed

332
Q

What is the treatment for broken arteries?

A

Bypass surgery can be done to fix blood flow and shunts can be put in place until surgery occurs

333
Q

What are the 3 layers of veins?

A

Adventia, media and intima

334
Q

How does the venous system get over gravity?

A

Helped by muscle pumps (venous pressure at ankle 100mmHg standing, 25mmHg walking). Also helped by the thoracic pump action during respiration and functioning competent valves.

335
Q

What is venous insufficiency and what are the symptoms?

A

Venous insufficiency is a common presentation. It is caused by failure of the muscle pump (typically the calf muscle) due to immobility, dependency, fixed ankle and loss of muscle mass or failure of valves.

Causes swelling and deep pigmented skin.

336
Q

What are the symptoms of venous hypertension?

A

Haemosiderin staining (brownish patch of skin)

Swollen legs

Itchy fragile sin

337
Q

What are the causes of venous hypertension?

A

Multifactorial;

  • Right heart failure
  • Liver failure
  • Compression of pelvic veins
  • Deep venous occlusion
  • Morbid obesity
  • Valve failure
  • Immobility
338
Q

What is the treatment of venous hypertension?

A

Treatment- emollient to stop skin cracks, compression (bandages, wraps and stockings). Also elevate and mobilise.

339
Q

What are the signs of valve failure?

A

Superficial veins= varicose veins

Deep veins= venous hypertension

340
Q

What is the treatment for valve failure?

A

Deep= compression or stockings

Superficial= vast majority of veins treated with an endothermal ablation technique, where in a vein below the knee is punctured and a catheter placed inside. A long wire is then passed under ultrasound guidance up the vein to the pelvis and the heating element inside the wire provides a thermal injury to the vein, resulting in venous injury and closure of the vein.

341
Q

What is foam sclerotherapy and what condition can it treat?

A

Foam sclerotherapy- needle inserted into the vein in the lower part of leg and a foamy mixture is injected in- bubbles of air are rapidly absorbed leaving behind a thin layer of sclerotherapy agent. Causes the vein to fibrose and occlude.

Alternate treatment for venous valve failure

342
Q

What is the porto-systemic venous system?

A

Mesenteric or portal venous drainage is via the liver before the heart

Systemic circulation returns to the heart directly

343
Q

What is portal hypertension?In liver disease the portal system fails to drain and portal hypertension develops. Blood is therefore diverted into the systemic venous system. Porto-systemic venous anastomosis is the name given to this.

A

In liver disease the portal system fails to drain and portal hypertension develops. Blood is therefore diverted into the systemic venous system. Porto-systemic venous anastomosis is the name given to this.

344
Q

What effects does portal-systemic hypertension have?

A

P-S hypertension can cause oesophageal varices where the portal system drains into the systemic venous system at the level of the diagram often into the oesophagus resulting in large distended veins just beneath the mucosal surface. If damaged or eroded will bleed heavily.

345
Q

What are the 3 layers of the lymphatic system?

A

Adventia, media and intima

346
Q

What is the structure of the lymphatic system?

A

Capillary structure

Valves like veins

Many anastomoses

347
Q

Where does the lympatic system drain to?

A

Capillaries drain to lymph nodes

Ultimately drain to the thoracic duct which empties into the left subclavian vein

348
Q

What are the main causes of lymphoedema?

A

Common in cancer patients when lymph node dissection occurs

Filariasis- parasitic worm infection that causes destruction of the lymphatic channels

349
Q

What are the treatment systems for lymphoedema?

A
  • compression
  • skin care
  • exercise
  • manual lymphatic drainage (massage techniques)
  • rarely surgery
350
Q

What can cause odema of the limbs?

A

Low oncotic pressure

Low protein (albumin)

Inflammation of the precapillary sphincter- vasodilated then more blood enters capillary system and so the leg becomes warm and swollen, tissue is hot to touch.

351
Q

What is special about heart muscle cells?

A
  • heart made of cardiomyocytes
  • contain 5000 mitochondria per cell
  • cells are aligned in sheets around the heart
352
Q

What is pre-load and what is it determined by?

A

The volume of blood in the ventricles at the end of diastole

Determined by: blood volume, capacity of the venous circulation to hold blood= venous tone

353
Q

What is afterload and what is it determined by?

A

Resistance the heart must overcome to circulate blood

Determined by tone in arterial circulation

354
Q

What is the vacular lining and what does it regulate?

A

The single cell layer lining in blood vessels

It regulates blood vessel tone, permeability, leukocyte adhesion and tendancy for thrombus formation

355
Q

What are the main causes of endothelial dysfunction?

A
  • elevated low density lipoprotein concentrations
  • Oxygen free radicals cause my smoking and inflammation
  • Infectious microorganisms such as the herpes virus
  • High blood pressure
356
Q

What are examples of drugs used for prevention of atheroma?

A
  1. statins
  2. Fibrates
  3. Ezectimbe
  4. PCSK9 inhibitors
357
Q

How do statins work and what is are examples?

A

Inhibit the enzyme HMG CoA reductase which inhibits mevalonate from being formed. Mevalonate forms cholesterol.

Examples= simvastatin, atorvastatin, pravastatin

358
Q

What are the side effects of statins?

A

SIDE EFFECTS= muscle pain, increased risk of diabetes, liver damage. In majority of people benefit in lipid lowering outweighs risk, but for some an alternative is required.

359
Q

How do Fibrates work and what are examples?

A

Fibrates e.g. bezafibrate, gemfibrozil, fenofibrate= decrease circulating very low density lipoprotein (VLDL) and triglyceride, only a small effect on LDL but also increase ‘protective’ high density lipoprotein (HDL)

360
Q

How is Ezetimbe used?

A

Lowers cholesterol absorption from small intestine via action in epithelial cells.

They are used with statins, or as an alternative to statins.

361
Q

How do PCSK9 inhibitors work?

A

increase LDL receptor recycling and availability on the cell surface and therefore increase LDL clearance.

362
Q

What is the treatment for acute attacks of angina?

A

Rest

Rapid acting organic nitrate, e.g. glyceryl trinitrate

363
Q

How does glyceryl trinitrate work?

A

Nitric oxide causes generation of cyclic GMP which relaxes smooth muscle cells

Glyceryl trinitrate can be used instead of NO as in injured tissue NO is not always produced

364
Q

What effects do nitrates have on the different areas of the blood vessels?

A
365
Q

What can occur with chronic use of glyceryl trinitrate?

A

Loss of tolerance and responsiveness

366
Q

What is Nicorandil?

A

A potassium channel opener

Means there is an increased polarisation in the cell- more negative as K leaves

This closes Na+ gates, calcium can no longer come into the cell and the smooth muscles relax

367
Q

What effects does Nicrorandil have on the CV system?

A

Reduces pre-load and afterload on heart and therefore O2 demand.

Dilates coronary arteries and can increase O2 supply

368
Q

What is nicorandil used to treat?

A

Angina

369
Q

What are the different drugs used to treat angina?

A

Glyceryl trinitrate

Nicorandil

B-antagonists

Calcium channel blockers

370
Q

What are the different types of anti-thrombotic drugs?

A

Anti-platelet= aspirin, clopidogrel and voripaxar

Anti-coagulation= warfarin and rivaroxaban

371
Q

How are platelets activated?

A

When there is a stimulus e.g. collagen or thrombin cycloxygenase converts arachidonic acid into cyclic endoperoxidases which through a number of steps activate platelets

Hence why COX inhibitors work

372
Q

What is an example og a cyclooxygenase inhibitor?

A

Asprin

373
Q

What is antithrombin 3?

A

Endothelial cells produce antithrombin 3, which also circulates in the plasma. It is the body’s own way of inhibiting the coagulation cascade

374
Q

How does unfractionated heparin and LMW heparin work and how is it administered?

A

Activates anti-thrombin III through binding to it

Cannot be taken orally, has to be intravenously

375
Q

What is the acute treatment for thrombosis?

A

Fibrinolytic clot buster drugs

Accelerate conversion of plasminogen to plasmin which degrades fibrin in thrombosis

376
Q

What are the effects of fibrinolytic clot buster drugs and how can these effects be reduced?

A

Can cause bleeding

Reversed by tranexamic acid

377
Q

What are the two types of heart failure?

A

Systolic heart failure= impaired contractibility and emptying of the ventricles

Diastolic= impaired relaxation and filling of the ventricle

378
Q

What are the mechanisms of cardiac glyosides?

A

Cardiac glycosides inhibit Na+/K+ ATPase pump. Accumulation of Na in cell stops the passive exchange mechanism and so calcium accumulates inside cells which leads to increased contractility

379
Q

What is an example of a cardiac glycoside?

A

Digoxin

380
Q

What is the problem with drugs that increase contracibility in heart failure?

A

They provide support in acute heart failure but also results in increased oxygen and energy demand so not helpful in chronic heart failure.

381
Q

What are two types of drugs that increase cardiac contracibility and used in heart failure?

A

Cardiac glyosides

B1- adrenoceptor

382
Q

How does the sympathetic system increase afterload and preload of the heart?

A
383
Q

What drugs are used for heart failure that involve the renin-angiotensin system?

A

ACE inhibitors e.g. enalapril and lisinopril

Also loop diuretics

384
Q

What blood tests can be done to work out the risk of heart disease?

A

Total cholesterol, LDL and HDL as well as C reactivity protein

385
Q

What is C-reactive protein?

A

Shows inflammation in the blood

Produced by liver and aipose tissue and assists in phagocytosis of damaged cells

386
Q

How is myocardial infarct diagnosed?

A

History of severe crushing pain, characteristic ECG changes and biomarkers

387
Q

What is troponin?

A

A component of the thin filament in striated muscle complexed to actin.

Regulates muscle contraction

There are specific cardiac isoforms which can be measured

388
Q

What is more sensitive; troponin levels or ECG?

A

For ECG changes, 5-10g of heart muscle needs to be lost

For troponin, only 0.003g

389
Q

What level of troponin will result in the diagnosis of a myocardial infarct?

A

Troponin blood levels > 99th percentile of the reference population

390
Q

Who has a higher 99th percentile for troponin, men or women?

A

Men

391
Q

What are natriuretic peptides?

A

Small proteins produced by heart muscle

As the heart muscle becomes more stretched there is an increased production

The hormones act to vasodilate and act in kidneys to increase amount of urine to lose blood volume to make the heart have to work less.

392
Q

What is BNP and Nt-proBNP?

A

A type of natriuretic peptide

Blood test can be used to diagnose heart failure after patient arrives with symptoms

393
Q

What are the problems with measuring natriuretic peptides to diagnose heart failure?

A

There is a problem with how specific it is- levels may rise due to arrythmias, respiratory disease and renal failure.

Not available in some areas of Scotland due to funding

Sem 2 Year 1 (12 decks)

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