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Medicine Phase One > Cardio-Respiratory Week Three > Flashcards

Cardio-Respiratory Week Three Flashcards

1
Q

Where do the coronary arteries arise?

A

Aortic sinus

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2
Q

What is the first branch of the right coronary artery?

A

Atrial branch. This gives of the sun-atrial branch

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3
Q

What branch right coronary artery goes around the front?

A

Right marginal branch

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4
Q

What branch of the right coronary artery goes around the back?

A

The posterior descending artery (interventricular)

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5
Q

What is the first branch of the left coronary artery?

A

Anterior interventricular artery (left anterior descending). This gives off the descending arteries.

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6
Q

What branch the left coronary artery goes around the back?

A

Circumflex artery. This gives of the left marginal branch

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7
Q

What are thebesian veins?

A

These are the veins that blood travels into from the sub-endocardium. These veins will then drain into the larger veins.

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8
Q

Where does the great cardiac vein originate and what artery does it follow?

A

The great cardiac vein (GCV) runs in the anterior interventricular groove and drains the anterior aspect of the heart where it is the venous complement of the left anterior descending artery.

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9
Q

Where does the small cardiac vein originate and what artery does it follow?

A

The small cardiac vein is a vein of the heart which accompanies the acute marginal artery from the RCA. It courses in the right posterior atrioventricular groove and drains into the coronary sinus close to it’s termination but may drain directly into the right atrium. It drains the right ventricle.

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10
Q

Where does the middle cardiac vein originate and what artery does it follow?

A

The middle cardiac vein or posterior interventricular vein is a vein of the heart which accompanies the posterior interventricular artery. It courses in the posterior interventricular groove and drains directly into the coronary sinus close to it’s termination. It drains the posterior wall of both ventricles and the posterior interventricular septum.

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11
Q

Where does the posterior vein of the left ventricle originate and what artery does it follow?

A

The posterior vein of the left ventricle is a vein of the heart which courses over the inferior wall of the left ventricle and drains into the coronary sinus to the left of where the middle cardiac vein drains into the sinus. It drains, not unsurprisingly, the inferior wall of the left ventricle.

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12
Q

Which set of veins drain directly into the right atrium?

A

anterior veins of the right ventricle

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13
Q

What are the venae cordis minimae?

A

A small group of veins that are within the walls of each chamber and drains directly into their respective chamber.

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14
Q

What is arteriosclerosis?

A

This is the thickening and hardening of the walls of the arteries

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15
Q

What is atherosclerosis?

A

This is the build-up of plaque in arteries which eventually causes hardening and narrowing of the arteries

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16
Q

How can the endothelium become damaged?

A

LDL, smoking, hypertension, irritants. These irritants cause the breakdown and allows LDL to enter the endothelium.

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17
Q

What does the endothelium release in response to irritants and what affect does this have?

A

The endothelium will resale ROS and MMPS. The macrophages will also release the same. This causes LDL oxidation.

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18
Q

How to foam cells develop?

A

These are formed by the macrophages. During the pathogenesis of atherosclerosis, macrophages will increase the expression of scavenger recepotrs in response to M-CSF. These will mediate LDL uptake and this forms foam cells.

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19
Q

What will foam cells release?

A

IGF-1: causes smooth muscle migration and proliferation

IL-1, IL-6 and TNF: inflammation and recruitment of more macrophages

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20
Q

Describe a fibrous cap, something that is present in atherosclerosis

A

This is formed by smooth muslce, proteoglycans and elastin. It overlies a fatty streak (dead foam cells). The smooth muslce Underneath will deposit calcium and this causes calcium crystals. Normally, the HDL will release the calcium but the accumulation of plaque messes with their ability. This results in calcium stiffening the walls.

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21
Q

What is the difference between fibrolipid plaques and fibrous plaques?

A

Fibrolipid plaques do not narrow the lumen as the muslce layer expands.
Fibrous plaques involves narrowing.

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22
Q

During, atherosclerosis, T cells will accumulate. They will release interferon-beta. What is the affect of this?

A

Inflammation

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23
Q

Describe the pain felt in angina pectoris

A

Pressure. Squeezing.

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24
Q

What is stable Angina?

A

This is the most common and pain will occur when the demand on the heart is increased, eg exercise. This will usually occurs with >70% stenosis. The pain will go away at rest.

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25
Q

What is unstable Angina?

A

There is pain present during rest and exercise. This is usually caused by a rupture of a plaque. This is an emergency and there is a high risk of MI.

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26
Q

What is Vasospastic Angina?

A

Ischaemia is a result of coronary artery vasospasm. There is constriction of smooth muscle and pain can occur at any time. Due to extreme contraction, all layers are affected and this causes transmural ischaemia.

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27
Q

What drugs can cause vasospasm of the heart and hence cause vasospastic angina?

A

Beta-adrenoreceptors

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28
Q

What is Prinzmetal’s angina another name for?

A

Vasospastic Angina

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29
Q

Give the mechanism of action of Organic nitrates

A

These mimic the actions of nitric oxide. They work directly on smooth muslce and cause dilation.
The nitrate groups on the drugs interact with enzymes and intracellular sulfhydryl groups to form NO. This stimulates the activation of guanylate cyclase and this forms cGMP. This causes dephosphoryalion of myosin light chains and this results in vasodilation.

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30
Q

What are the overall effects of organic nitrates?

A

There is vasodilation of large veins.

Increase cGMP inhibits calcium entry and hence causes dilation.

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31
Q

Organic nitrates give a higher dilation of veins than arteries, what is the significance of this?

A

Venous dilations predomination means that venous preload and pressure id decrease. This reduces ventricular wall stress and therefore oxygen demand by the heart decreases.
Systemic arterioles dilation will reduce afterload and this will also reduce ventricular wall stress.

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32
Q

What enzyme converts nitro-glycerine into NO?

A

Aldehyde dehydrogenase

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33
Q

What is the timing of nitro-glycerine?

A

It works within 2-5 minutes and wears off within 30 minutes.

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34
Q

Why is nitro-glycerine given sublingually?

A

If it is given orally, it will be heavily metabolised by the first-pass effect

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35
Q

How long should the nitro-glycerine free period last?

A

Over 8 hours

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36
Q

Give two examples of long-acting nitrates

A

Isosorbide dinitrate ( 4-6 hours ) and Isosorbide mononitrate ( 6-8 hours) . These are taken orally due to no first pass effect.

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37
Q

Why do organic nitrates cause a headache?

A

Dilation of cerebral arteries

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38
Q

What kind of drug is Verapamil?

A

Calcium-Channel blocker

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39
Q

What kind of drug is Diltiazem?

A

Calcium-Channel blocker

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40
Q

What kind of drug is Amlodipine?

A

Calcium-Channel blocker

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41
Q

What kind of drug is Nifedipine?

A

Calcium-Channel blocker

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42
Q

What are the two mechanisms is which calcium L-channel blockers work?

A

Open channel block: the pore in which calcium travels through is blocker
Allosteric modulation: drugs binds to the allosteric site and causes shape change which limits the opening

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43
Q

Give examples of Open calcium- channel blockers

A

Verapamil and Diltiazem

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44
Q

Give examples of allosteric modulation calcium blockers?

A

Amlodipine and nifedipine

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45
Q

Out of the following drugs, which is best form smooth muslce and which is best of cardiac muslce?

A

Smooth muslce: nifedipine, diltiazem, verapamil.

Cardiac muscle: verapamil, diltiazem, nifedipine

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46
Q

Give examples of non-selective beta blockers

A

Propranolol, nadolol, pindolol

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47
Q

Give examples of selective beta blockers

A

Atenolol, metaprolol, nebrulol

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48
Q

Describe the beta-one receptors in the heart

A

When these become activated, they form cAMP and this increase calcium, resulting in increased heart rate and contraction.

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49
Q

Describe the beta-two receptors blood vessels

A

There is increases smooth muslce relaxation.

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50
Q

What is the mechanism of action of Ranolazine?

A

This blocks inward sodium channels in cardiomyocytes. Increased sodium would lead to increase calcium through the sodium-calcium exchanger. By blocking the receptor, there is a prevention of calcium overload and hence reduced myocardial oxygen demand.

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51
Q

What is the mechanism of action of Ivabradine?

A

This blocks ‘If’ channels (funny channels). These are located in the SA node and are responsible for cardiac pacemaker activity and by blocking them, there is a reduction heart rate and a reduction in myocardial demand.

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52
Q

What is the mechanism of action of Nicorandil?

A

This activates potassium channels and causes vasodilation.

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53
Q

What enzyme do statins inhibit?

A

HMG CoA reductase

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54
Q

What is HMG CoA reductase responsible for? This is the enzyme that statins inhibit

A

HMG CoA reductase is involved in cholesterol synthesis. Activation of this enzyme causes activation of SREBP, a transcription factor that up-regulates the LDL receptor.

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55
Q

PCI is surgery used to treat heart conditions. What is it?

A

PCI is percutaneous coronary intervention. This is where a fine guide is placed across the coronary stenosis and a balloon is inflated. This dilates the stenosis. A coronary scent is placed for ‘scaffolding’.

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56
Q

What causes the pain in Angina?

A

A build up of metabolites (potassium, carbon dioxide, lactate, adenosine) which activate sensory nerves and causes the pain.

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57
Q

What is the difference between cAMP and cGMP.

A

These are both secondary messengers.
cAMP is synthesized from ATP by adenylyl cyclase and its synthesis is stimulated by G proteins.
cGMP is synthesized from GTP by guanylyl cyclase and its synthesis is active by nitric oxides.

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58
Q

On an ECG, what does a P wave represent?

A

Atrial depolarization

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59
Q

On an ECG, what does a P-R interval represent?

A

Delay through AV node

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60
Q

On an ECG, what does a QRS complex represent?

A

Ventricular depolarization

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61
Q

On an ECG, what does a T wave represent?

A

Ventricular repolarization

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62
Q

On an ECG, what does a ST segment represent?

A

The isoelectric period where both ventricle are depolarized.

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63
Q

On an ECG, what does a U wave represent?

A

Purkinje repolarization

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64
Q

On an ECG, what does a QT interval represent?

A

Time taken for both ventricular depolarization and repolarization to occur

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65
Q

Where are the six chest electrodes placed on the heart for an ECG?

A

V1: right 4th intercostal space
V2: left 4th intercostal space
V3: midway between V2 and V4
V4: midclavicular line in 5th intercostal space
V5: same level as V4 on left anterior axillary midline
V6: same level as V4/5 on left mid-axillary line

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66
Q

What plane and the chest and limb electrodes on?

A

Chest: transverse
Limb: coronal

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67
Q

How many seconds does one small square equal on an ecg?

A

0.04 seconds

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68
Q

What view of the heart does chest electrodes V1 and V2 give?

A

Septal

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69
Q

What view of the heart does chest electrodes V3 and V4 give?

A

Anterior

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70
Q

What view of the heart does chest electrodes V5 and V6 give?

A

Lateral

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71
Q

What is the normal axis of the heart?

A

+90 to -30

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72
Q

What is the axis for left an right heart deviation?

A

Left: -90 to -30
Right: +90 to +180

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73
Q

For the limb leads, what represent lead one, two and three?

A

Lead one: aVR and aVL
Lead two: aVR and aVF
Led three: aVL and aVF

74
Q

What does no P waves represent?

A

Atrial fibrillation

75
Q

What leads does the heart conduction tend to flow to?

A

Leads one, two and three. Lead two will be the most positive.

76
Q

What is the most negative lead from the heart conduction direction?

A

aVR

77
Q

Describe right axis deviation

A

This is usually carries out by right ventricular hypertrophy. There is the new axis of +90 to +180. More muscles means there will be more positive signal and hence lead three will be ore positive.
RAD is commonly associated with pulmonary conditions as they strain the heart.

78
Q

Describe left axis deviation

A

The new axis is -30 to -90. Lead one will become more positive and lead three becomes mores negatives.
LAD is usually caused by conduction defects rather than the mass of the ventricle.

79
Q

How do you calculate the heart rate from looking at an ecg?

A

Count the number of large squares within one R-R internal. Divide this by 300.

80
Q

What is the normal duration of a P-R interval?

A

120-200 ms (3-5 small squares)

81
Q

What does prolonged PR interval mean?

A

AV block

82
Q

What does a shortened PR interval mean?

A

The conduction takes less time. There is a short accessory pathway and this will show a delta wave.

83
Q

What is the normal duration of a QRS complex?

A

0.12 seconds

84
Q

What is a sign of Wolff Parkinson white syndrome?

A

Delta wave

85
Q

What doe tall QRS complexes imply?

A

Ventricular hypertrophy

86
Q

What is the difference between ST elevation and depression?

A

Elevation: acute full thickness MI
Depression: myocardial ischaemia

87
Q

What is the difference between STEMI and NON-STEMI?

A

STEMI: ST elevation MI caused by sudden blockage of a coronary artery
NON-STEMI: caused by severally narrowed artery but not completely blocker

88
Q

Considering all the leads, which ones give an inferior view of the heart and what is their associated artery?

A

Leads II, III aVF

Right Coronary artery

89
Q

Considering all the leads, which ones give a lateral view of the heart and what is their associated artery?

A

Leads i, aVL, V5 and V6

Left circumflex artery

90
Q

Considering all the leads, which ones give an anterior view of the heart and what is their associated artery?

A

Leads V3 and V4

Left anterior descending

91
Q

Considering all the leads, which ones give a septal view of the heart and what is their associated artery?

A

Leafs V1 and V2

Left anterior descending

92
Q

Where is the nucleus placed in cardiac muscle?

A

Centrally

93
Q

What node is responsible fro transmitting signals from atria to ventricles?

A

SA node

94
Q

When heparin binds to Antithrombin III, what factors will they inhibit?

A

IIa, IXa, Xa, XIa, XIIa

95
Q

What does low molecular heparin usually inhibit?

A

Xa

96
Q

What property does heperan have to have in order to inhibit thrombin (IIa)?

A

The molecule must be long enough to bond to both Antithrombin and thrombin. Most of the chain of LMWH are not long enough

97
Q

What molecule does heparin bind to?

A

Antithrombin III

98
Q

Low molecular wright heparin has a lowed incidence of HIT. What is HIT?

A

Heparin-induced thrombocytopenia: Low blood platelet count as a result of the medication heparin.

99
Q

Can heparin cross the placenta of blood-brain barrier?

A

No

100
Q

How is heparin given?

A

Intravenously or sub-cutaneously

101
Q

What is the mechanism of action of protamine?

A

This is a heparin antagonist that reverse the side effects of heparin

102
Q

What is the function of reduced vitamin K in the coagulation cascade?

A

This is essential for post-ribosomal gamma-carboxylation of glutamic acid at factors II, VII, IX and X

103
Q

What is the mechanism of action of warfarin?

A

Blocks vitamin K reductase. This means that factors II, VII, IX and X cant be made

104
Q

Why is the effects of warfarin delayed?

A

It takes 1-3 days form the existing pool of functional clotting factor to b replaced by dysfunctional ones

105
Q

What protein does warfarin bind to?

A

Albumin

106
Q

What is the mechanism of action of dabigatran etexilate?

A

Blocks thrombin (factor IIa)

107
Q

What drug inhibits Factor IIa directly?

A

Dabigatran etexilate

108
Q

What is the mechanism of action of Rivaroxaban?

A

Inhibits Factor Xa

109
Q

What drug inhibit factor Xa directly?

A

Rivaroxaban

110
Q

What is the mechanism of action of aspirin?

A

Inversely inhibits COX and this inhibits the production of thromboxane A2 in platelets (this cant be reversed as platelets have no nucleus). This also inhibits endothelial production of prostaglandin, but this can be reversed due to no production of COZ

111
Q

What is the mechanism of action of dipyridamole?

A

This inhibits the enzyme cyclic nucleotide phosphodiesterase, preventing cAMP degradation. cAMP is a platelet inactivator.

112
Q

What is the mechanism of action of epoprostenol?

A

This is given intravenously. This is used during haemodialysis. this is an analogue of PGI2 and causes cAMP production, hence platelet inhibition.

113
Q

What is the mechanism of action of clopldogrel?

A

This blocks ADP binding and hence GPIIb/IIIa exposure. This reduces platelet aggregation.

114
Q

What is the mechanism of action of Abclximbab?

A

This binds and blocks GPIIb/IIIa recepotrs.

115
Q

What is the function of tPA?

A

This is an enzyme produced by vascualr endothelium which activates plasminogen.

116
Q

What is the mechanism of action of Streptokinase?

A

This activates plasminogen.

117
Q

What is the mechanism of action of tranexamic acid?

A

Plasminogen activator inhibitor

118
Q

What is the name of factor I?

A

Fibrogen

119
Q

What is the name of factor II?

A

Porthrombin

120
Q

What is the name of factor III?

A

Tissue thromboplastin

121
Q

What is the name of factor IV?

A

Calcium

122
Q

What is the name of factor V?

A

Labile factor

123
Q

What is the name of factor VII?

A

Stable factor

124
Q

What is the name of factor VIII?

A

Anti-haemophilic A

125
Q

What is the name of factor IX?

A

Christmas factor

126
Q

What is the name of factor X?

A

Stuart power factor

127
Q

What is the name of factor XI?

A

Plasmin-thromboplastin antecedent

128
Q

What is the name of factor XII?

A

Hageman factor

129
Q

What is the name of factor XIII?

A

Fibrin stabilizer factor

130
Q

Which factor is labile factor?

A

V

131
Q

Which factor is fibrinogen?

A

I

132
Q

What factor is Stuart power factor?

A

X

133
Q

What is the mnemonic for the clotting factors?

A

Foolish people try climbing long slopes, after charismas some people have fallen

134
Q

What are unipolar leads?

A

Measure potential variation at single point between one limb and neutral electrode

135
Q

What are bipolar leads?

A

Measure between two leads

136
Q

Are limbs leads bipolar or unipolar?

A

Bipolar

137
Q

Are chest leads bipolar or unipolar?

A

Unipolar

138
Q

Are augmented leads bipolar or unipolar?

A

Unipolar

139
Q

What happens during right bundle branch block?

A

Signals will be sent from the SA node, to atria, to AV ode, to bundle of HIS. The left ventricle will contract first and then its signals will go to the right ventricle as it is blocked.

140
Q

What will happen to the QRS complex when there is a bundle Branch block?

A

The QRS complex will start normally but be delayed.

141
Q

What is the ECG finding in left bundle branch block?

A

The overall depolarization will come from the right side and move to the left. This means it goes toward V6. This creates a negative VI and a positive V6. V6 will be notched due to left ventricle depolarizing late.

142
Q

What is the ECG finding in right bundle branch block?

A

The first part of the conduction system is normal as the septum depolarizes first, causing a slight positive VI and slight negative V6. The left ventricle will then depolarise and cause a positive V6 and negative V1. There will then be a negative V6 and a positive Vi as the right ventricle depolarizes. V6 will have a slurred S wave and V1 has a terminal R wave.

143
Q

What is the mnemonic for bundle branch block?

A

William Marrow: left to right (V1 to V6)

144
Q

What are the two parts of the atrium that the crista terminal separates?

A
  • Sinus venarum (posterior to crista and receives blood from vena cave. There are smooth muscles)
  • Atrium proper (anterior to crista. IT has right auricle and has rough walls due to pectinate muscles)
145
Q

What part of the mediastinum is the thoracic duct and oesophagus in?

A

Posterior

146
Q

What are the four main tracheobronchial lymph nodes?

A

Tracheal. Bronchial. Bronchopulmonary. Pulmonary.

147
Q

Where is trabeculae carnae located?

A

Rough walls on ventricles

148
Q

Where is the moderator band found?

A

Right ventricle

149
Q

What is the venous angel (where the thoracic duct enters the venous system)?

A

The junction between internal jugular ad subclavian

150
Q

What are the tributaries of the azygous vein?

A
  • posterior intercostal veins
  • hemiazygous
  • accessory hemiazygous
  • right ascending lumbar vein
151
Q

What is a ventricular septal defect?

A

Hole in the heart

152
Q

What is the remnant of the ductus arteriosus?

A

Ligementum arteriosum

153
Q

What is the remnant of the ductus venosus?

A

Ligementum venosum

154
Q

What is the remnant of the foramen ovale?

A

Fossa ovalis

155
Q

What is a probe patent foramen ovale?

A

unfused fossa ovalis

156
Q

What happens to the P and Q wave during exercise?

A

Increase

157
Q

What happens to the T wave and QT terminal and R wave and PR segment during exercise?

A

Decreases

158
Q

Will there be ST elevation or depression with transmural ischaemia?

A

Elevation

159
Q

Will there be ST elevation or depression with subendochrondal ischaemia?

A

Depression

160
Q

What is the function of PGI1 in regards to platelets?

A

Inhibits them

161
Q

What synthesis vWF?

A

Endothelial cells

162
Q

What is deficient in haemophilia A?

A

Factor VIII

163
Q

What is deficient in haemophilia B? (Christmas disease)

A

Factor IX

164
Q

What is deficient in haemophilia C?

A

Factor XI

165
Q

What cells are platelet fragments of?

A

Megakaryocytes

166
Q

What is the disorder called where there is a low platelet count?

A

Thrombocytopenia

167
Q

What is Glanzmann thrombasthenia?

A

Abnormal GPIIb/IIIa

168
Q

What is the colour difference in a venous and arterial clot?

A

Venous s red and arterial is white

169
Q

What are some functions of cholesterol?

A
  • cell membranes
  • maintain fluidity and permeability
  • steroids and fat-soluble vitamins
170
Q

Describe the exogenous pathway of cholesterol

A

Dietary fats and fatty acids absorbed in small intestine. Triglycerides are formed in the enterocytes from free fatty acids and cholesterol. They form chylomicrons. They travel via the lymph and are taken up by tissues for energy or fat storage. Remnants are taken up by the liver for HDL synthesis.

171
Q

Describe the endogenous pathway of cholesterol

A

VLDL is formed in the liver from triglycerides and cholesterol esters. Once used for energy, it is transformed into LDL. LDL ins internalized in the liver and is secreted into the intestines.

172
Q

What is familial hypercholesterolemia?

A

Familial hypercholesterolemia is a genetic disorder. It is caused by a defect on chromosome 19. The defect makes the body unable to remove low density lipoprotein (LDL, or bad) cholesterol from the blood. This results in a high level of LDL in the blood.

173
Q

What is Xanthomas?

A

Cholesterol deposits on skin

174
Q

What is Xanthelosmas?

A

Cholesterol deposits around eye

175
Q

What is Arcus senilis?

A

White rig around cornea

176
Q

What is the final pathway of lymph before the veins?

A

Supraclavicular lymph nodes

177
Q

What is the clinical significance of ‘Virchow’s node’?

A

This is the left supraclavicular node. Swelling will shows abdominal malignancy.

178
Q

What is absolute risk?

A

Incidence of disease in given population

179
Q

What is relative risk?

A

Comparing absolute is to exposure

180
Q

What is attribute risk?

A

Difference between exposed and unexposed

181
Q

What is the Brain-bridge reflex?

A

The Bainbridge reflex, also called the atrial reflex, is an increase in heart rate due to an increase in central venous pressure. Increased blood volume is detected by stretch receptors (Cardiac Receptors) located in both atria at the venoatrial junctions.

Medicine Phase One (44 decks)

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