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Medicine Year 2 (Bear) > Myocardial Infection (M.I) > Flashcards

Myocardial Infection (M.I) Flashcards

0
Q

Fesicular breath sounds are?

A

Normal breath sounds.

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1
Q

The presenting complaint should be written in the ____ _____

A

Patients words

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2
Q

Acute coronary syndromes include?

A

ST-Elevation myocaridal infarction (STEMI) Non ST- Elevation myocardial infarction (NSTEMI) Unstable Angina (UA)

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3
Q

What is the difference between NSTEMI and UA?

A

In NSTEMI there is occluding thrombus, which leads to myocardial necrosis and a rise in serum troponins or CK-MB.

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4
Q

When does Myocardial infarction occur?

A

When cardiac myocytes die due to myocardial ischaemia.

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5
Q

What is a Type 1 Myocardial infarction?

A

Spontaneous MI with Ischaemia due to a primary coronary event, e.g. plaque erosion/rupture, fissuring or dissection.

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6
Q

What is a type 2 MI?

A

MI secondary to Ischaemia due to increased oxygen demand or decreased supply, such as coronary spasm, coronary embolism, anaemia, arrhythmias, hypertension or hypotension.

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7
Q

What are type 3 MI’s?

A

Diagnosis of MI in sudden cardiac death.

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9
Q

What are type 4a MI’s?

A

Diagnosis of MI after percutaneous coronary intervention (PCI). Trop x5 >99th centile)

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10
Q

What is a type 5 MI?

A

Diagnosis of MI after Coronary artery bypass graft (CABG). Trop x 10 >99th centile

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11
Q

What is the common mechanism to acute coronary syndrome?

A

Rupture or erosion of the fibrous cap of a coronary artery plaque. This leads to platelet aggregation and adhesion, localised thrombosis, vasoconstriction and distal thrombus embolisation. Thrombus formation, and the vasoconstriction produced by platelet release of serotonin and thromboxane A2 results in myocardial ischaemia due to reduction of coronary blood flow.

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12
Q

In pleural effusion, tracheal deviation is ___. Expansion is ___, the percussion note is ____Tactile vocal phremetis and breath sounds are _____.

A

Away from the effusion. Reduced Stony Dull Decreased

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13
Q

In pneumothorax tracheal deviation is ___. Expansion is ___, the percussion note is ____Tactile vocal phremetis and breath sounds are _____.

A

Central in normal - Away in Tension Decreased Hyperresonant Decreased

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14
Q

In Lung collapse tracheal deviation is ___. Expansion is ___, the percussion note is ____Tactile vocal phremetis is _____and breath sounds are _____.

A

Towards the collapsed lung Decreased or equal Dull Reduced Reduced or absent

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15
Q

In Pneumonia tracheal deviation is ___. Expansion is ___, the percussion note is ____Tactile vocal phremetis and breath sounds are _____. Added sounds are ____ and/or ____

A

Central Equal or decreased Dull Increased (bronchial breathing) Crackles - Coarse Pleural Rub

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16
Q

In COPD tracheal deviation is ___. Expansion is ___, the percussion note is ____Tactile vocal phremetis and breath sounds are _____. Added sounds are ____.

A

Central Hyper-inflated, equal, but expands less Hyperresonant Decreased Expiratory polyphonic wheeze

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17
Q

In ABG, you must perform which test, and why?

A

Allen’s test - to check that hand perfusion is suitable from ulnar artery alone.

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18
Q

What does JACCOL stand for in note taking?

A

Jaundice, anaemia, clubbing, cyanosis, oedema or lymphadenopathy.

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19
Q

Anosmia is an abnormality of which cranial nerve?

A

1 - Olfactory

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20
Q

Partial sight/blindness, scotoma, aniscoria and optic disk changes are all signs of a problem with which cranial nerve?

A

II - Optic

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21
Q

Impaired or lost accommodation reflex, strabismus, diplopia and nystagmus indicate a problem with which cranial nerves?

A

III - Oculomotor IV - Trochlear VI - Abducens

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22
Q

Impaired or distorted facial sensation, corneal reflex, and weakness of chewing movement indicate a problem with which cranial nerve?

A

V - Trigeminal

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23
Q

Facial weakness, and loss of or change in taste at the front of the tongue indicate a problem with which cranial nerve?

A

VII - Facial

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24
Q

A Lower motor neuron lesion does not spare the forehead - true or false?

A

True. an UMN spares it.

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25
Q

Impaired hearing or deafness, and vertigo indicate a problem with which cranial nerve?

A

VIII - Vestibulocochlear

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26
Q

A loss of pharyngeal sensation would show a problem with which cranial nerve?

A

IX Glossopharyngeal

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27
Q

Impaired palate movements indicate a problem with which cranial nerve?

A

X - Vagus

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28
Q

Weakness of neck movement is suggestive of a problem with which cranial nerve?

A

XI - Accessory

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29
Q

Dysarthria and chewing/swallowing problems indicate a problem with which cranial nerve?

A

XII - Hypoglossal

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30
Q

What three signs would you see in the face of a px with bells palsy?

A

smooth forehead eyebrow droop Droop of the corner of the mouth

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31
Q

What is the maximum length for a normal PR interval?

A

200 ms

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32
Q

What is the maximum length of time for a normal QRS segment?

A

120 ms

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33
Q

What is the maximum length of time for a normal QT segment?

A

450ms

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34
Q

Two signs of Atrial fibrillation on ECG?

A

No P-waves Rhythm-irregularly irregular

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35
Q

What is paroxysmal atrial fibrillation?

A

Atrial fibrillation present for less than seven days

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36
Q

What is persistent AF?

A

Present for > 7 days - may be reverted back to sinus rhythm

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37
Q

What is permanent AF?

A

As name suggests, cannot be reverted back to sinus rhythm.

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38
Q

Which two drugs could you use to control rhythm in AF?

A

Flecanide Amiodarone

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39
Q

Which drugs could you use to control RATE in AF?

A

Beta blockers, calcium channel blockers (diltiazem, verapamil), digoxin

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40
Q

A saw toothed ECG baseline is indicative of what?

A

Atrial flutter P waves at rate of approx 300 Usually with 2:1 block, but other blocks can be seen. Carries a sim. stroke risk to AF.

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41
Q

What causes atrial flutter?

A

Re-entry circuit within the right atrium.

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42
Q

Bifid P waves indicate what?

A

Left atrial hypertrophy.

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43
Q

Name a cause of left atrial hypertrophy.

A

Mitral stenosis, aortic stenosis, mitral regurgitation

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44
Q

Short PR interval, sinus, Broad QRS with a slurred upstroke of the Q wave (this is otherwise known as a delta wave) on ECG is a sign of what?

A

Wolff-Parkinson- White Syndrome. Due to an accessory pathway.

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45
Q

An ECG showing increased R wave in V4-V6 and increased S wave in V1-V3 is indicative of what?

A

Left ventricular hypertrophy

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46
Q

What qualifies as ST elevation?

A

Elevation of the ST segment above the baseline. To qualify, should be more than 2 small squares above baseline in chest (precordial) leads, or more than 1 small square above baseline in limb leads.

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47
Q

What can ST depression indicate?

A

NSTEMI Unstable angina

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48
Q

Anterior STEMi results from occlusion of which artery?

A

Left anterior descending

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49
Q

The lateral wall of the left ventricle is supplied by which arteries?

A

Left anterior descending and circumflex arteries.

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50
Q

In lateral STEMI, what would you expect of the T waves?

A

Tall/hyperacute

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51
Q

In an inferior STEMI, which leads would you expect ST elevation in?

A

II, III, and AVF.

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52
Q

Which artery is occluded in an inferior STEMI?

A

Posterior interventricular artery

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53
Q

Inferior MI’s account for what percentage of all Myocardial infarctions?

A

40-50%

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54
Q

What may cause widespread ST elevation throughout the precordial and limb leads?

A

Pericarditis

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55
Q

Name some causes of pericarditis.

A

Dressler’s syndrome (4-6 post MI) Infection Immune or drug related

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56
Q

What is prolonged QT interval, and what risk does it pose?

A

Delayed Repolarisation of the heart following a heartbeat, increasing the risk of torsades de pointes.

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57
Q

What is the treatment for prolonged QT long-term?

A

implantable cardioverter-defibrillator

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58
Q

What does Hyperkalaemia cause?

A

Prolonged PR interval Broad and bizarre QRS complexes *PEAKED T WAVES - MAY LOSE P WAVE*

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59
Q

QRS positive in leads I and AVL, negative in leads II and AVF - what is this?

A

Left axis deviation

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60
Q

What causes left axis deviation?

A

Left ventricular hypertrophy Left bundle branch block

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61
Q

QRS positive in leads III and AVF, and negative in leads I and AVL. What is this?

A

Right axis deviation

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62
Q

Name some causes of Right axis deviation

A

Right ventricular hypertrophy Pulmonary embolism COPD

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63
Q

Pulseless electrical activity - will a shock help?

A

NO!

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64
Q

Asystole - “flat lining”. Besides making sure everyone is watching how cool you’re about to be, what do you do?

A

This is a non-shockable rhythm Give adrenaline (1mg) once IV access and then every 3-5 minutes following. After all, YOLO.

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65
Q

VF and VT are both what?

A

Shockable rhythms

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66
Q

With reagrds to the JVP, what is the A wave?

A

This is first peak. It is caused by back pressure in the Jugular vein during atrial contraction.

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67
Q

With regards to the JVP, what is the X wave?

A

The drop in pressure, caused during atrial relaxation.

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68
Q

With regards to the JVP, what is the C peak?

A

A small increase in pressure (small pressure wave), caused by closure of the tricuspid valve.

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69
Q

With regards to the JVP, what is the X prime wave?

A

This is a pressure drop, caused by the right Ventricular contraction.

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70
Q

With regards to the JVP, what is the V wave?

A

Venous filling with a closed tricuspid valve, causing an increase in pressure.

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71
Q

With regards to the JVP, what is the Y descent?

A

A drop in venous pressure, as a response to atrial emptying.

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72
Q

What is the JVP?

A

A measurement of the pressure in the internal jugular vein, as an extension of the R atrium

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73
Q

What would cause a decrease in JVP in a normal heart?

A

Atrial relaxation Tricuspid valve open

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74
Q

What does an a wave represent?

A

Atrial contraction

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75
Q

Just preceding the C wave (JVP), what happens?

A

Closure of tricuspid valve due to ventricular systole.

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76
Q

Specifically, what does the X wave represent?

A

Atrial relaxation

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77
Q

What is the y descent?

A

Blood from the atrium, going to the ventricle.

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78
Q

What is the V wave?

A

Specifically, filling of the right atrium. Think “Villing!”

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79
Q

What is the order of wave forms in the JVP?

A

A,C,X,V,Y

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80
Q

What change in the JVP would you expect to see in pulmonary hypertension (Tricuspid stenosis, pulmonic stenosis)

A

Increased/Higher a wave. May also see lessening of the Y wave

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81
Q

What changes in JVP might we see in AF?

A

There would not be an a wave There would be no x descent (no atrial relaxation)

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82
Q

What would you see in JVP with Complete heart block (3rd degree heart block/VT)?

A

A Cannon a wave - a huge increase in the a wave, very high on physical examination. This is due to atria contracting on a closed Tricuspid valve. It’s due to AV dysynchrony.

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83
Q

What do you see in the JVP if a patient has tricuspid regurgitation?

A

A CV wave. This is a lack of the X descent, instead having a positive wave from C to V.

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84
Q

What happens to JVP in tamponade?

A

Reduced atrial relaxation, causing loss of y descent. This is because when blood leave R atrium to R ventricle, external fluid shifts and compresses R atrium, resulting in loss of Y descent.

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85
Q

What happens to JVP in constrictive pericarditis?

A

Constrictive paricarditis is a fibrous “wall” that prevents expansion of right ventricle. This means that the Y descent is a very sharp, and deep y descent, quickly returning to baseline. This is sometimes known as a square root descent.

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86
Q

Sphenoid sinus drainage and posterior ethmoid drainage meet where?

A

The Sphenoethmoidal recess

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87
Q

Where does the frontal sinus drain to?

A

Anterior Hiatus semilunaris

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88
Q

Where do the anterior ethmoid air cells drain into?

A

The Ethmoid bullae

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89
Q

Where does the maxillary sinus drain to?

A

Hiatus semilunaris

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90
Q

A 32 year old man presents to his GP with a 2 day history of dyspnoea and retrosternal chest pain which came on gradually. No history of trauma or abnormal exertion, and the patient has never been ill before. The pain is stabbing in quality, radiates to the neck and left shoulder, is relieved by sitting upright, and is made worse by lying flat and coughing.

A

Pericarditis. It may seem a bit like reflux, but it’s retrosternal, and stabbing in quality.

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91
Q

A 35 year old man has been brought to A&E by ambulance having collapsed at work. His chest pain began 40 minutes ago and has worsened gradually. It is now in a tight band across his chest and radiates to his neck but not his arms. On examination, he is grey, sweaty and short of breath with a pulse of 40 beats per minute. What do you suspect?

A

Myocardial Infarction

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92
Q

A 67 year old hypertensive obese man brought to A&E having collapsed whilst moving a cupboard. Chest pain began suddenly when lifting is central, severe, burning and tearing in quality, and radiates through to his back and up to his neck. BP 190/120 Right arm, and 160/90 left arm. What did you suspect?

A

Dissecting thoracic aortic aneurysm

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93
Q

A 68 year old female presents with heavy central chest pain radiating to her left arm which began an hour ago and woke her from sleep. The pain is similar to, but more severe than her usual angina, and her GTN spray has not relieved it. She is admitted to hospital where serial troponin T tests are negative. What is this?

A

Unstable angina.

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94
Q

A 38 year old female with SLE presents to A&E with a 24 hour history of sharp, right sided chest pain which is made worse by deep inspiration. She is not short of breath. She suffered a miscarriage five days ago, necessitating overnight admission to hospital for evacuation of retained products of conception. Since leaving hospital her left leg has become swollen, warm and tender to palpation. What is this?

A

This is pulmonary embolism. Loads of thrombotic risk factors.

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95
Q

Name the two branches of the Opthalmic division of the trigeminal cranial nerve (CNVI).

A

The frontal nerve Nasociliary nerve

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96
Q

Name the two branches of the frontal nerve

A

Supraorbital nerve Supratrochlear nerve

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97
Q

Name the two branches of the Nasociliary nerve

A

Anterior ethmoidal nerve Posterior ethmoidal nerve

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98
Q

Which muscle does the Frontal nerve sit on the superior aspect of when crossing the orbit?

A

IT crosses the superior aspect of levator palpebrae superioris muscle.

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99
Q

Which three nerves are parts of the maxillary division of the trigeminal cranial nerve (CN V2)?

A

The maxillary division gives off the zygomatic nerve, then two pterygopalatine nerves.

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100
Q

Sensory fibres from the pterygopalatine ganglion supply the nose, paranasal sinuses and palate as:?

A

Pterygopalantine nerves Nasopalatine nerves Greater and Lesser palantine nerves

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101
Q

When does the maxillary division become the infraorbital nerve?

A

As it enters the infraorbital canal. Just before this canal, it gives off the posterior superior alveolar nerve.

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102
Q

Which two divisions of infraorbital nerve exit the infraorbital canal along its route?

A

Middle superior alveolar nerve Anterior superior alveolar nerve

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103
Q

What is the Pterygopalantine ganglion?

A

It’s a knot of nerve fibres found in the pterygopalantine fossa. It allows parasympathetic from the greater petrosal nerve of the facial nerve and sympatheti fibres from the deep petrosal nerve of the internal carotid plexus to pass along fibres of the Maxillary branch of the trigeminal nerve (CN VII).

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104
Q

What do the sympathetic and parasympatheitc fibres of the pterygopalatine ganglion control?

A

Lacrimation Nasal secretions Nasal airflow

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105
Q

Lacrimation is controlled by?

A

Zygomatic nerve

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106
Q

Nasal secretions are controlled by which nerves?

A

Pterygopalantine, nasopalantine and greater palantine nerves.

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107
Q

What is nasal airflow controlled by (nerve)?

A

It is controlled via the pterygopalantine nerve to turbinates on the lateral nasal wall.

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108
Q

Which nerve supplies the frontal sinuses?

A

Branches of the supraorbital nerves (CN V1)

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109
Q

Which nerves supply the Ethmoid sinuses?

A

Branches of the nasociliary nerves (anterior and posterior ethmoidal nerves)

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110
Q

Which nerve supplies the Sphenoidal sinuses?

A

Branches of the nasociliary nerves (Posterior ethmoidal nerve)

111
Q

Which nerves supply the maxillary sinuses?

A

Branches of the maxillary nerve.: Greater palantine nerve Posterior superior alveolar nerve Infraorbital nerve

112
Q

Olfaction is supplied by which nerve?

A

Olfactory cranial nerve

113
Q

How many bundles of olfactory neurosensory cells are on either side of the lateral and septal wall of the nasal cavity?

A
  1. These pass through the cribiform plate foramina in tubes of dura and arachnoid mater to enter the olfactory bulbs in the anterior cranial fossa.
114
Q

Which nerves supply the nasal septum?

A

Nasociliary nerves (CN VI) and branches of the maxillary nerve (CN VII)

115
Q

Which nerves supply the lateral nasal wall?

A

Branches of the nasociliary nerve (CN VI) Branches of maxillary nerve (CN VII)

116
Q

Name the respiratory related causes of central chest pain.

A

Pulmonary Embolism Pneumothorax Pleurisy

117
Q

Name cardiac causes of chest pain.

A

Angina Pericarditis Myocardial Infarction

118
Q

Alimentary causes of chest pain?

A

Oesophagitis Oesophageal spasm Oesophageal rupture

119
Q

Musculoskeletal causes of chest pain?

A

Costochondritis Fractured Ribs Nerve compression

120
Q

Vascular causes of chest pain?

A

Aortic dissection Intramural thrombus

121
Q

What is Ischaemia?

A

It’s reversible - no harm done.

122
Q

What is Infarction?

A

Irreversible, cell death (troponin release)

123
Q

What is the most common cause of both cardiac ischaemia and cardiac infarction?

A

Coronary atheromatous disease

124
Q

What do you need to diagnose acute myocardial infarction?

A

Symptoms characteristic of myocardial pain: Characteristic alteration in electrophysiological properties of the ischaemic myocardium. Evidence of cardiac myocyte necrosis In clinical practice, evidence of myocyte necrosis is required to confirm acute myocardial infarction.

125
Q

Which features of chest pain increase the likelihood of MI?

A

Radiation R shoulder 2.9 Radiation L arm 2.3 Both L + R arm 7.1 Pain in chest/L arm 2.7 Chest pain most impt symptom 2.0

126
Q

Which features decrease the probability of an MI?

A

Pleuritic 0.2 Sharp/stabbing 0.3 Positional 0.3 Reproduced by palpation 0.2-0.4

127
Q

What is silent Myocardial infarction?

A

Undiagnosed typical symptoms Unrecognised typical symptoms Atypical symptoms esp elderly, diabetic

128
Q

What are the signs of Acute Myocardial infarction?

A

No specific physical signs Looks anxious during pain, sweating, pale Excess sympathetic tone,hypertension,tachycardia Excess parasympathetic tone,bradycardia,hypotension, nausea, belching, Impaired LV function, hypotension, crackles in lungs, 3rd heart sound, murmurs

129
Q

What are the treatment principles of an MI?

A

1.) Support and monitor - Oxygen, analgesia, ECG monitor. 2.) Confirm diagnosis - ECG, Blood markers 3.) Open the artery and restore blood flow. - Percutaneous coronary intervention & Thrombolysis. 4.) Protect the heart and vessels - B blockers, ACE-Inhibitors; Antiplatelets 5.) Rehab and prevention - Long term. Cessation of smoke, exercise, statin etc.

130
Q

Which artery does an angiogram enter through?

A

Originally Femoral artery, now technological advances have allowed for use of radial artery (smaller calibre, but less compx).

131
Q

Which gender is a higher risk factor for CAD?

A

Male

132
Q

What role does the endothelium have in the vessel?

A

Release of Nitrous Oxide: Vasodilation, Growth inhib. Integrity, Antithrombotic, and Leukoinhibitory (prevents white cells sticking to vessel wall).

133
Q

What are the pathological input signals that contribute to Endothelial Dysfunction?

A

See slide (Friday first lecture)

134
Q

See This study: Relationship of endothelium dependent casodilation to vascular risk factors in asymptomatic ___?

A

D o tiq

135
Q

What effects do an increased sheer force gradient, and intravasculuar haematological turbulence have on the endothelium?

A

They increase the release of inflammatory markers, and associated atherosclerotic changes.

136
Q

Low risk of a cardiac event is defined by what?

A

10% risk over the next ten years.

137
Q

What effect does CRP have on the risk of cardiac events?

A

An increased CRP increases the risk of cardiovascular event in a similar way to conventional risk factors (i.e. smoking, drinking, poor diet etc)

138
Q

Which risk prevention strategies have evidence for improved outcomes in CVD patients?

A

See slide - near end - 1st lecture friday

139
Q

What effect does lowering SBP have on pre-CVD patients?

A

Greatly reduces risk of Coronary or thromboembolic events.

140
Q

What use is an ECG during acute coronary events?

A

Useful to ID complicating arrhythmias, i.e. VF or VT, AF, or Heart block(s). Will show evidence of previous MI will show dynamic ST segment change

141
Q

What does dynamic ST segment change determine and detect?

A

Determines need for reperfusion therapy Determines response to therapy Detects recurrent ischaemia

142
Q

Where is the J point on an ECG?

A

The J point occurs at the end of the QRS complex.

143
Q

What is ST elevation an indication for?

A

Reperfusion therapy (PCI/Thrombolysis).

144
Q

what is ST elevation taken to mean?

A

Complete coronary occlusion

145
Q

Can MI occur in the absence of ST segment change?

A

YES.

146
Q

If ST elevation is a marker of complete coronary occlusion, what is ST depression associated with?

A

Incomplete occlusion (usually).

147
Q

Cardiac enzymes are markers of what?

A

Cardiac myocyte necrosis

148
Q

Cardiac enzymes may not become elevated in peripheral circulation until __-__ hours after the onset of the event.

A

4-6

149
Q

What are the clinical uses of cardiac enzymes?

A

Diagnostic and prognostic.

150
Q

CK-MB cardiac enzyme tends to peak ____ than Cardiac ____ after Acute myocardial infarction.

A

CK-MB cardiac enzyme tends to peak sooner than Cardiac Troponin after Acute myocardial infarction.

151
Q

Cardiac enzymes tend to peak __-___ days after Acute MI

A

1-2

152
Q

Why is raised Troponin NOT DIAGNOSTIC of AMI?

A

Troponin is elevated in a variety of clinical cases (i.e. PE, septicaemia, renal failure), so is only a confirmatory marker.

153
Q

What non-acute coronary syndrome causes of troponin elevation are there?

A

Renal dysfunction, Congestive heart failure, Hypertensive crisis, PA, Tachy/Brady arrhythmias, myocarditis, stroke, AAA, Hypothyroidism, Tako-Tsubo cardiomyopathy, infiltrative diseases (i.e. haemochromatosis), drug TOx, burns, Rhabdomyolysis, critical systemic illness.

154
Q

What is a Type 4b MI?

A

MI associated with verified stent thrombosis.

155
Q

What are the criteria for acute MI types 1 & 2?

A

Detection of rise and/or fall of cardiac biomarkers (pref. troponin) with at least one value above the 99th percentile of the upper reference limit, together with evidence of ISCHAEMIA, AND EITHER: - ECG changes of new Ischaemia, or pathological Q waves on ECG. - Imaging evidence of new loss of viable myocardium/wall abnormality.

156
Q

When deciding on the need for reperfusion therapy the working diagnosis is what?

A

ACS with or without ST elevation.

157
Q

the diagnosis of infarction requires elevated _ _____.

A

cardiac enzymes

158
Q

Often, the diagnosis of MI is confirmed only ___ ___ ___ ___.

A

after the initiation of treatment.

159
Q

What are the aims the management of MI?

A

Reduce risk of death, reduce damage done, promote healing, reduce further event risk.

160
Q

Which intervention improved prompt recognition of MI symptoms?

A

Public education - and professional!

161
Q

Which intervention improved provision of heart monitoring & resuscitation?

A

Ambu 999 response, Hospital cardiac care units.

162
Q

Which intervention improved restoration of coronary blood flow?

A

Reperfusion tx: Primary angioplasty and thrombolytic therapy., nitrates, and elective angioplasty/CABG.

163
Q

Which intervention improved prevention of further coronary thrombosis post MI?

A

Anticoagulants and anti-platelet agents.

164
Q

Which intervention improved reduction and reversal of ischaemia?

A

Reperfusion tx, Anti-anginal drugs (i.e. B- blockers, nitrates).

165
Q

Which intervention improved stabilisation of coronary artery?

A

Statins

166
Q

Which intervention improved optimised healing?

A

ACE inhibitors

167
Q

Which intervention improved prevention of future MI?

A

Secondary prevention drugs and lifestyle changes.

168
Q

Which intervention improved education and support/promotion of healthy lifestyles post-mi?

A

Hospital cardiac care specialists, cardiac rehab classes and patient support groups.

169
Q

What does LMWH Heparin work on?

A

Factor Xa and thrombin.

170
Q

What does Bivalirudin work on?

A

Thrombin

171
Q

what does Fondaparinux work on>?

A

Factor Xa

172
Q

Anticoagulation therapy aims to prevent the production of what?

A

Thrombus (Fibrin)

173
Q

Antiplatelet therapy aims to reduce what?

A

Thrombus (platelet aggregation).

174
Q

Clopidogrel, Prasugrel, Ticagrelor and GPIIb/IIIa inhibitora are what?

A

Antiplatelet agents.

175
Q

In a STEMI (as opposed to a NSTEMI), which two additional treatments occur?

A

Fibrinolytic therapy Immediate percutaneous intervention.

176
Q

How many people were admitted with heart attack in England and Wales in 2012?

A

80,974

177
Q

More than half of all heart attacks occur in persons over the age of ___.

A

70

178
Q

What is the aim of reperfusion treatment?

A

Restoration of patency of a completely occluded artery as quickly as possible.

179
Q

What are the advantages of thrombolytic drugs in STEMI?

A

established Trx, simple, widely available inc. pre-hospital.

180
Q

What are the disadvantages of thrombolytic drugs in STEMI?

A

Fails in at least 20% Risk of bleeding/stroke

181
Q

What are the advantages of Primary PCI in STEMI?

A

Successful in at least 95%, lower stroke risk, allows visualisation, cardiologist involvement, evidence based.

182
Q

What are the disadvantages of Primary PCI in STEMI?

A

Not available in all centres, risk of bleeding, Trx delayed until arrival at hospital.

183
Q

Blood lipids are mainly made up of ___ and ___

A

Fatty acids and cholesterol.

184
Q

Blood lipids are mostly transported in a protein capsule called a ____

A

lipoprotein.

185
Q

What is hyperlipidaemia?

A

The presence of elevated or abnormal levels of lipids and/or lipoproteins in the blood, and is a major risk factor for cardiovascular disease.

186
Q

What are Chylomicrons?

A

These are lipoproteins. They carry fats from the intestine. In the liver, chylomicron particles release triglycerides and some cholesterol.

187
Q

What is VLDL?

A

Very low density lipoprotein.

188
Q

With regards to VLDL: The liver converts unburned food metabolites into__ ___ ___ ______ and secretes them into _____where they are converted to _____ density lipoproteins, then __ ___ _____ particles and non ______fatty acids.

A

The liver converts unburned food metabolites into v low density lipoproteins and secretes them into plasma where they are converted to Intermediate density lipoproteins. then LDL particles and non esterified fatty acids.

189
Q

Healthy individuals have relatively few ___ particles, which are ___.

A

Few Large

190
Q

In atheromatous disease, there are large numbers of ___ ____ ____ particles, within the arteries. for this reason, it is referred to as ___ cholesterol.

A

In atheromatous disease, there are large numbers of small dense LDL particles, within the arteries. for this reason, it is referred to as bad cholesterol.

191
Q

HDL particles transport ____ back to the liver for ___. For this reason they are called ___ cholesterol.

A

HDL particles transport cholesterol back to the liver for excretion. For this reason they are called good cholesterol.

192
Q

In the intestine, short and medium chain fatty acids are absorbed directly into the blood via the ___ ___.

A

Portal vein

193
Q

In the intestine, long-chain fatty acids are coated with cholesterol and proteins to form ____.

A

chylomicrons.

194
Q

At the intestine, chylomicrons enter the lymphatic capillaries and enter the bloodstream at the ___ ___ ____, avoiding the ___.

A

Left subclavian vein Avoiding the liver

195
Q

Insulin stimulates the uptake of fatty acids in certain cells after a meal. In which cells does this happen?

A

Liver cells, adipocytes, muscle cells.

196
Q

some of the fatty acids taken up liver cells are converted into ___ and again secreted into the blood.

A

VLDL

197
Q

Several hours after the last meal, fatty acids in the ___ decrease, causing ____ to release stored fatty acids into the blood as free fatty acids, in order to supply cells with energy via fatty acid oxidation.

A

Several hours after the last meal, fatty acids in the blood decrease, causing adipocytes to release stored fatty acids into the blood as free fatty acids, in order to supply cells with energy via fatty acid oxidation.

198
Q

an increase in chylomicrons or VLDL leads to an increase in ___.

A

Triglyceride.

199
Q

An increase in low density lipoproteins, or intermediate density lipoproteins leads to an increase in _____.

A

cholesterol.

200
Q

In type 1 primary hyperlipidaemia ____are elevated. Associated clinical disorders include ___ and ___.

A

In type 1 primary hyperlipidaemia chylomicrons are elevated. Associated clinical diusorders include Lipoprotein lipase deficiency and apolipoprotein C-II deficiency.

201
Q

In type IIa primary hyperlipidaemia ____are elevated. Associated clinical disorders include: _____________________________

A

LDL. Familial hypercholesterolemia, polygenic hypercholesterolemia, nephrosis, hypothyroidism and familial combined hyperlipidaemia.

202
Q

In type IIb primary hyperlipidaemia ____are elevated. Associated clinical disorders include

A

LDL, VDL. Familial combined hyperlipidemia

203
Q

In type III primary hyperlipidaemia ____are elevated. Associated clinical disorders include:

A

IDL Dysbetalipoproteinemia

204
Q

In type IV primary hyperlipidaemia ____are elevated. Associated clinical disorders include:

A

VLDL Familial hypertriglyceridemia, familial combined hyperlipidemia, sporadic hypertriglyceridemia, diabetes.

205
Q

In type V primary hyperlipidaemia ____are elevated. Associated clinical disorders include:

A

Chylomicrons, VLDL Diabetes

206
Q

What is secondary hyperlipidaemia?

A

Hypertriglyceridaemia most commonly due to a secondary cause. It is often important to treat the cause rather than the Hypertriglyceridaemia. May be assoc. with abdo pain, recurrent fever and jaundice.

207
Q

What examples of conditions associated with secondary hyperlipidaemia can you remember?

A

Nephrotic syndrome Hypothyroidism Biliary Obstruction

208
Q

What is the principal plasma abnormality of Heterozygous familial hypercholesterolemia?

A

+LDL only (inherited abnormality of the LDL receptor) [IIa]

209
Q

What is the principal plasma abnormality of Familial defective apolipoprotein B?

A

+LDL (inherited abnormality of apoprotein B interferes with binding to LDL receptor) [IIa]

210
Q

What is the principal plasma abnormality of Familial combined hyperlipidemia ?

A

1/3: LDL only [IIa] •1/3: VLDL only [IV] •1/3: LDL and VLDL [IIb] Apo-B overproduction is common

211
Q

What is the principal plasma abnormality of Polygenic hypercholesterolemia?

A

+LDL [IIa]

212
Q

What is the principal plasma abnormality of Familial hypertriglyceridemia (2.3-10 mmol/L)?

A

+VLDL only (high VLDL production, decreased lipoprotein lipase activity) [IV]

213
Q

What is the principal plasma abnormality of Severe hypertriglyceridemia ( TG >10 mmol/L))?

A

+Chylomicrons and VLDL (high VLDL production, decreased lipoprotein lipase activity) [V]

214
Q

What is the principal plasma abnormality of Familial hypoalpha- lipoproteinemia?

A

reduced HDL (< 0.78 mmol/L) in males; <0.90 mmol/L) in females) (decreased apo A-1 production)

215
Q

What is the principal plasma abnormality of Dysbetalipoproteinemia?

A

+IDL, +chylomicron remnants

216
Q

What are the clinical features of Heterozygous familial hypercholesterolemia and Familial defective apolipoprotein B?

A

•tendinous xanthomas •corneal arcus •premature CAD •family history of hypercholesterolemia

217
Q

What are the clinical features of Polygenic hypercholesterolemia?

A

•premature Cardiac risk •no xanthomas •no family history of hypercholesterolemia

218
Q

What are the clinical features of Familial combined hyperlipidemia ?

A

•usually >30 yr old •often overweight •usually no xanthomas •premature CAD •different generations have different lipoprotein abnormalities

219
Q

What are the clinical features of Familial hypertriglyceridemia?

A

•often overweight •>30 yr old •often diabetic •hyperuriaemic •may or may not have premature CAD •determined by family history and HDL-C

220
Q

What are the clinical features of Severe hypertriglyceridemia?

A

•usually middle-aged •often obese •often hyperuricaemic •usually diabetic •risk for recurrent pancreatitis

221
Q

What are the clinical features of Familial hypoalpha- lipoproteinemia?

A

•premature CAD (cardiac events)

222
Q

What are the clinical features of Dysbetalipoproteinemia?

A

•yellow palmar creases •palmar xanthomas •tuberoeruptive xanthomas •premature CAD

223
Q

Cholesterol is a constituent of ___ and a source of ___ _____.

A

Cholesterol is a constituent of membranes and a source of steroid hormones.

224
Q

Ideal cholesterol level in the blood is?

A

<5mmol/l

225
Q

mildly high cholesterol level?

A

5 - 6.4mmol/l.

226
Q

moderately high cholesterol level?

A

6.5 - 7.8mmol/l.

227
Q

very high cholesterol level?

A

above 7.8mmol/l.

228
Q

Aspirin (acetylsalicylic acid) exerts anti-platelet action through irreversible _____ of platelet ______ (COX)-1 .

A

Aspirin (acetylsalicylic acid) exerts anti-platelet action through irreversible acetylation of platelet cyclooxygenase (COX)-1 .

229
Q

Platelet cyclooxygenase (COX)-1 is responsible for conversion of arachadonic acid to various ___

A

eicosanoids.

230
Q

What is thromboxane A2?

A

This is produced from arachadonic acid (it’s an eicosanoid). It is a potent vasoconstrictor and platelet agonist. Production of TXA2 has been completely inhibited by doses of aspirin as low as 100 mg.

231
Q

Prostaglandin I2 (prostacyclin) is a _____ and platelet _____ produced both by _____ and vascular ______.

A

Prostaglandin I2 (prostacyclin) is a vasodilator and platelet inhibitor produced both by platelets and vascular endothelium.

232
Q

Once acetylated by aspirin, COX-1 is permanently _____ and, as anucleate cells, platelets cannot ____ the defective enzyme. This effectively halts platelet _____ production for the entire ____day life span of the platelet.

A

Once acetylated by aspirin, COX-1 is permanently deactivated and, as anucleate cells, platelets cannot replace the defective enzyme. This effectively halts platelet TXA2 production for the entire 10-day life span of the platelet.

233
Q

Familial Hypercholesterolaemia is a Autosomal dominant disorder of chromosome 19 with homozygous and heterozygous forms; Defined in the WHO as a type IIa hyperlipidaemia.

A

Familial Hypercholesterolaemia is a Autosomal dominant disorder of chromosome 19 with homozygous and heterozygous forms; . Defined as a type IIa hyperlipidaemia.

234
Q

Tendon xanthomata are virtually diagnostic of_________?

A

heterozygous familial hypercholesterolaemia

235
Q

What are tendon xanthomata?

A

Free mobile papules or nodules in the tendons, ligaments, fascia and periosteum especially on the backs of the hands, fingers, elbows, knees and heels

236
Q

What is a Xanthelasma?

A

The appearance of yellow flat plaques over the upper or lower eyelids, most often near the inner canthus.

237
Q

what is corneal arcus?

A

A grey opaque line which surrounds the margin of the cornea, separated from it by an area of clear cornea.

238
Q

How do you diagnose definite familial hypercholesterolaemia?

A

total cholesterol above 7.5 mmol/l (in adults) OR LDL cholesterol above 4.9 mmol/l (in adults) PLUS tendon xanthomata in patient or 1st or 2nd degree relative.

239
Q

LDL receptor is coded on chromosome ___

A

19.

240
Q

what is the usual function of LDL receptors?

A

to allow LDL to be taken up by cells from the tissue fluid.

241
Q

•Familial Hypercholesterolaemia (FH) occurs due to a mutation in the LDL receptor which prevents ___ ___ __ ______

A

•Familial Hypercholesterolaemia (FH) occurs due to a mutation in the LDL receptor which prevents efficient uptake of LDL.

242
Q

what is the main (non drug) treatment for hyperlipidaemia?

A

Low lipid diet - maintain lean weight.

243
Q

The first-line treatment of familial hypercholesterolaemia is a _____?

A

The first-line treatment of familial hypercholesterolaemia is a statin. Evidence that high statin doses, e.g. atorvastatin 80 mg daily, may reverse intimal thickening in FH.

244
Q

HMG CoA reductase inhibitors are otherwise known as what?

A

Statins

245
Q

what are the actions of statins?

A

• inhibition of hydroxymethylglutaryl coenzyme A (HMG CoA) in the liver. • reduction in plasma cholesterol and LDL • increase in LDL receptors • small reduction in plasma triglyceride and VLDL • modest increase in HDL

246
Q

What class of drugs are ciprofibrate, gemfibrizil and fenofibrate?

A

Fibrates.

247
Q

What are the main actions of fibrates?

A

Main actions: decrease serum triglyceride and increase HDL. Particularly effective at reducing the circulating concentration of small, dense LDL.

248
Q

Fibrins should be used with caution in patients with ___ ____

A

Renal impairment - may increase creatinine levels.

249
Q

What is Polygenic hypercholesterolaemia and familial combined hyperlipidaemia?

A

• Increased hepatic secretion of VLDL particles associated with both PH and FCH • LDL production is increased and LDL-receptor mechanism often overloaded.

250
Q

With reference to the arterial wall, what is the intima?

A

Endothelium with basal lamina (basement membrane) Subendothelial connective tissue - collagen, elastic fibres, smooth muscle Internal (fenestrated) elastic lamina Endothelium = simple squamous cells

251
Q

With reference to the arterial wall, what is the Media?

A

Thickest layer Elastic fibres, collagen Smooth muscle cells Few fibroblasts

252
Q

With reference to the arterial wall, what is the Adventitia?

A

Connective tissue and fibroblasts Thinner than media Some elastic fibres Prevents over-stretch of arterial wall Vasa vasorum and nervi vascularis.

253
Q

The hallmark of atheromatous disease is ___ _____.

A

Endothelial dysfunction, leading to: • adherence of platelets and wbc’s to the endothelium, • passage of inflammatory wbc’s into the subendothelial space, • accumulation of lipid-rich cells, smooth muscle cells and new blood vessel growth

254
Q

What are the Main components of atheromatous plaques?

A

Connective tissue matrix – Collagen, proteoglycans, fibronectin, elastic fibres • Crystalline cholesterol, cholesteryl esters, phospholipids • Cells – Monocyte-derived macrophages, smooth muscle cells, T-lymphocytes, dendritic (antigen presenting) cells • Thrombotic material (platelets/fibrin)

255
Q

“The endothelium is a dynamic_____ and paracrine organ that regulates anti-______, mitogenic and contractile activities of the vessel____, as well as the ______ process within the vessel lumen”

A

“The endothelium is a dynamic autocrine and paracrine organ that regulates anti-inflammatory, mitogenic and contractile activities of the vessel wall, as well as the haemostatic process within the vessel lumen”

256
Q

What are the products from endothelial cells?

A

Nitric Oxide and Adhesion moleules.

257
Q

What are the products from inflammatory cells?

A

– Cytokines, growth factors, metalloproteinases

258
Q

What are the products from vascular smooth muscle cells?

A

– Proteinases, growth factors, collagen,elastin

259
Q

What are the Potential anti-atherogenic actions of NO?

A

• Inhibition of smooth muscle proliferation • Inhibition of monocyte adhesion to, and migration through, endothelium • Anti-platelet effects • Promotion of macrophage apoptosis in plaque • Inhibition of lipid oxidation

260
Q

Atherosclerotic disease has a long___ ____.

A

Atherosclerotic disease has a long incubation period

261
Q

What is the order of progression of atherosclerosis?

A

Fat streak Inflammatory cell migration/activation Smooth muscle recruitment Fibrous cap Plaque erosion/rupture Platelets Thrombosis

262
Q

Thrombosis occurs due to either ___ or ____ of the ___ ____ of the plaque.

A

Thrombosis occurs due to either erosion or rupture of the fibrous cap of the plaque.

263
Q

Plaques at risk of future thrombotic events are characterised by what?

A

• Large lipid cores (>50% overall plaque volumes) • Thin caps in which collagen structure is disorganised • High densities of macrophages and high levels of expression of tissue factor and metalloproteinases • Low densities of smooth muscle cells • Large numbers of vasa vasorum at the base with rupture of internal elastic lamina

264
Q

What are the Characteristics of an Unstable plaque?

A

Inflammatory cells, thin cap, eroded endothelium, activated macrophages and few SMCs.

265
Q

The outcome of atherosclerosis is determined more by the ______ of the plaque, than by its _____.

A

The outcome of atherosclerosis is determined more by the composition of the plaque, than by its size.

266
Q

Atherosclerotic lesions frequently _____ as a consequence of repeated subclinical episodes of rupture and repair.

A

Atherosclerotic lesions frequently enlarge as a consequence of repeated subclinical episodes of rupture and repair.

267
Q

A 55 YO man with 4 hours of crushing chest pain has just arrived. This is his ECG. What do you see?

A

Acute inferior myocardial infarction

ST elevation in the inferior leads II, III and aVF
reciprocal ST depression in the anterior leads.

Right Bundle Branch Block and sinus bradycardia are also present.

268
Q

A 63 year old woman with 10 hours of chest pain and sweating. This is their ECG. What do you see?

A

Acute anterior myocardial infarction

ST elevation in the anterior leads V1 - 6, I and aVL
reciprocal ST depression in the inferior leads

269
Q

A 60 year old woman with 3 hours of chest pain arrives in A& E. this is their ECG. what do you see?

A

Acute posterior myocardial infarction

(hyperacute) the mirror image of acute injury in leads V1 - 3
(fully evolved) tall R wave, tall upright T wave in leads V1 -3
usually associated with inferior and/or lateral wall MI

270
Q

A 53 year old man with Ischaemic Heart Disease is a new patient at your GP surgery. A routine ECG is done - what can you see?

A

Old inferior myocardial infarction

a Q wave in lead III wider than 1 mm (1 small square) and
a Q wave in lead aVF wider than 0.5 mm and
a Q wave of any size in lead II

271
Q

A 79 year old man with 5 hours of chest pain present to A & E. An ECG is done. What do you see?

A

Acute myocardial infarction in the presence of left bundle branch block
Features suggesting acute MI

ST changes in the same direction as the QRS (as shown here)
ST elevation more than you’d expect from LBBB alone (e.g. > 5 mm in leads V1 - 3)
Q waves in two consecutive lateral leads (indicating anteroseptal MI)

272
Q

Name the parts of the external nose.

A
273
Q

Identify the paranasal sinuses.

A
274
Q

Explain the innervation of the paranasal sinuses in relation to referred pain.

A

It is useful to know that the sinuses may cause diagnostic difficulties due to referred pain: the maxillary sinus is innervated by the infraorbital nerve and anterior, middle and posterior superior alveolar nerves. Hence, pathology here may be felt as upper jaw pain, toothache or pain in the skin of the cheek.

Medicine Year 2 (Bear) (30 decks)

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