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Year 2 > Case 4 > Flashcards

Case 4 Flashcards

1
Q

Why is endothelium significant in the clotting cascade?

A

Synthesis of von Willibrand factor (haemostasis) and PGI2 (antithrombotic, prevents aggregation of platelets)

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2
Q

Production of nitric oxide by endothelial cells

A

Ligand binds to GPCR. Activation of PLC which converts PIP2 to IP3 and DAG.
These molecules cause an increase in intracellular Ca2+.
Ca2+ binds to calmodulin and activates eNOS (endothelial NO synthase).
eNOS synthesises NO from L-arginine - BH4 is an essential cofactor.

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3
Q

How is NO production maintained when stimulus is prolonged?

A

Increased transcription of eNOS.

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4
Q

How do endothelial cells in the blood vessel walls respond to mechanical force?

A

Glycocalyces project into lumen of vessel and are attached to the cytoskeleton. Movement of glycocalyx activates Ca2+ channels. Increased Ca2+ intracellularly causing eNOS activation. NO production and vasodilation.

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5
Q

How does NO cause vasodilation?

A

Activation of cGMP and therefore PKG. PKG inhibits Ca2+ influx into sarcoplasm and promotes Ca2+ efflux out of sarcoplasm.
(PKG also inhibits IP3 mediated Ca2+ influx pathway)

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6
Q

Paracrine effects of Nitric Oxide

A

Decreased platelet aggregation + decreased monocyte and platelet adhesion
Decreased LDL oxidation - fewer atheromatous plaques formed.
Decreased expression of adhesion molecules
Decreased smooth muscle proliferation and contraction.

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7
Q

Changes in vascular endothelial cells with age

A

Older endothelial cells generate more reactive oxygen species.
ROS react with NO, reducing its bioavailability and producing peroxinitrites which have detrimental effects on cell functions.
Endothelial dysfunction - reduced vasodilation

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8
Q

Changes to blood vessels which occur as a result of endothelial dysfunction

A

Thickening of media and narrowing of lumen (due to vascular inflammation and remodelling)
Increased stiffness and potentially calcification.

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9
Q

Endothelium derived contracting factors

A

Usually prostanoids which cause contraction.

Has a greater effect when NO production is impaired.

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10
Q

Risk factors for atherosclerosis

A 
Smoking 
Hyperlipidaemia 
Diabetes 
Hypertension 
Shear stress (occurs at sites where blood changes speed/direction)
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11
Q

Formation of an atheromatous plaque

A

Circulating LDL and monocytes cross the vascular endothelium into the intima.
LDLs become oxidised (oxidised LDL promotes increased permeability of endothelium)
Monocytes mature into macrophages.
Macrophages take up OxLDL and become foam cells.
Foam cells release inflammatory signals to recruit more leukocytes to site.
Foam cells accumulate and become apoptotic - releasing LDL and forming a lipid deposit. This also causes proinflammatory signal release, so further influx of inflammatory cells.
Finally, smooth muscle cells dedifferentiate, migrate and proliferate into intima. Secrete ECM forming a fibrous cap.

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12
Q

Factors responsible for monocyte adhesion to vascular endothelial cell membrane

A

P selections and E selectins

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13
Q

Factors responsible for monocyte migration across vascular endothelial cell membrane into intima

A

MCP-1 and OxLDL

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14
Q

Why does atheromatous plaque formation occur at regions where blood changes direction/speed?

A

Part of the wall will experience a decrease in shear stress - less eNOS activation.
Therefore, less endothelial repair.
More ROS generated, leukocyte adhesion, LDL entering intima and inflammation.

When the plaque is formed, the region of disturbed flow is amplified.

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15
Q

Eccentric plaque

A

Does not occupy the whole circumference

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16
Q

Concentric plaque

A

Occupies the whole circumference

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17
Q

Factors which affect stability of atheromatous plaques

A

Size - larger plaques contain more soft material and are therefore less stable.
Lipid content - higher ratio of lipid to fibrous cap is less stable
Bleeding inside the cap - increased pressure and therefore more susceptible to rupture.

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18
Q

Endothelial contracting factors

A 
H2O2
Prostanoids 
Angiotensin II
Endothelin - I
Thromboxane A2
Superoxide anion
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19
Q

Endothelial relaxing factors

A 
NO
PGI2
H2O2
Adenosine 
Epoxyeicosatrienicacids (EETs)
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20
Q

Endothelium Derived Hyperpolarising Factor

A

Compensatory mechanism - cause vasodilation when NO bioavailability is compromised due to superoxide production.
Significant role in disease states e.g. hypertension

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21
Q

Left Anterior Descending coronary artery supplies…

A

Right and left ventricles and interventricular septum

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22
Q

Left Marginal coronary artery supplies…

A

Left ventricle

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23
Q

Left circumflex coronary artery supplies…

A

Left atrium and ventricle

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24
Q

Right Coronary artery supplies…

A

Right atrium and ventricle

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25
Q

Right Marginal Coronary artery supplies…

A

Right ventricle and apex

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26
Q

Posterior Interventricular coronary artery supplies…

A

Right and left ventricles and interventricular septum

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27
Q

RCA occlusion causing MI on an ECG

A

Inferior MI

ST elevation in II, III and aVF

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28
Q

LAD occlusion causing MI on an ECG

A

Septal MI - ST elevation in V1 and V2

Anterior MI - ST elevation in V3 and V4

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29
Q

LCx occlusion causing MI on an ECG

A

Lateral MI - ST elevation in I, aVL, V5 and V6

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30
Q

Composition of lipoproteins

A

Lipid core - Triglyceride and cholesteryl esters

Surface coat - phospholipid, unesterified cholesterol and apolipoproteins.

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31
Q

Function of HDL

A

Transport cholesterol back to liver

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32
Q

Apolipoprotein associated with HDL

A

ApoA1 (receptor ligand)

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33
Q

Apolipoprotein associated with LDL

A

ApoB100 (receptor ligand)

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34
Q

Function of LDL

A

Transport cholesterol from liver to tissues

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35
Q

Function of IDL

A

Transport cholesterol from liver to tissues

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36
Q

Apolipoprotein associated with IDL

A

ApoE (receptor ligand)

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37
Q

Function of VLDL

A

Transport cholesterol from liver to tissues

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38
Q

Apolipoprotein associated with VLDL

A

ApoCII (cofactor lipoprotein lipase)

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39
Q

Function of chylomicrons

A

Transport triglyceride from gut to liver

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40
Q

Apolipoprotein associated with chylomicrons

A

ApoB48 (Receptor ligand)

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41
Q

What are apolipoproteins?

A

Proteins that bind lipids to form lipoproteins - transport lipids through lymphatics and circulatory system.

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42
Q

Exogenous lipid transport pathway

A

Fat and cholesterol absorbed from GI tract assembled to form chylomicrons.
Chylomicrons carried in the bloodstream, deposit their fats when they meet tissues expressing Lipoprotein lipase (e.g. Adipose)
Remaining chylomicron remnant used to form empty HDL or are removed at the liver by binding of ApoE to their receptor.

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43
Q

Endogenous lipid transport pathway

A

Fatty acids in liver (transported here OR synthesised) packaged into VLDLs.
VLDLs carried in the bloodstream, deposit their fats when they meet tissues expressing Lipoprotein lipase (e.g. Adipose)
They are now called IDLs, which are absorbed into liver, broken down into LDLs by hepatic lipase.
Circulating LDLs are absorbed into various tissues on binding to their receptors.

HDL created as a biproduct.

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44
Q

Reverse cholesterol transport pathway

A

Too much cholesterol in peripheral tissue causes activation of ABCA1 receptor.
HDL interacts with this receptor causing LDL to be returned to the liver.
Antiatherogenic

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45
Q

When do patients with atherosclerosis become symptomatic?

A

Development of fibrous cap - increased risk of complications such as plaque rupture, thrombosis and haemorrhage

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46
Q

Familial Hypercholesterolaemia

A

Insufficient (heterozygote) or no (homozygote) ApoB100 receptor for LDL to bind to so that it is removed from circulation.
Autosomal dominant.
Causes development of cardiovascular disease 20yrs early.

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47
Q

Treatment of familial hypercholesterolaemia

A

Statins

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48
Q

Clinical signs for hypercholesterolaemia

A

Xanthelasma
Tendon Xanthoma
Corneal Arcus

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49
Q

PCSK9

A

Enzyme which binds to LDL receptor and breaks it down so that it is unable to remove LDLs.
Inhibited by certain drugs to lower serum cholesterol.

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50
Q

Cholesterol synthesis

A

Acetyl coA converted to HMG CoA.
HMG CoA converted to mevalonate by HMG CoA Reductase.
Mevalonate then converted to cholesterol

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51
Q

ADRs of statins

A 
Nasopharyngitis
Hyperglycaemia 
Headache 
Pharyngolaryngeal pain 
Epistaxis 
GI disorders 
Musculoskeletal and connective tissue disorders (Myositis in 2-3%)
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52
Q

Contraindications of statins

A

Active liver disease
Raised AST or ALT
Pregnancy or breastfeeding

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53
Q

Most commonly used statin

A

Atorvastatin

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54
Q

Statin used in children

A

Pravastatin

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55
Q

Indication for statins

A

Primary prevention - patients at high risk of CVD

Secondary prevention - patients who have had an MI already

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56
Q

Dicrotic notch

A

Sudden dip in pressure in aorta due to backflow of blood in artery as valve closes (AKA Incisura)

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57
Q

Effect of atherosclerosis on dicrotic notch

A

Larger - less compliant blood vessel, cannot compensate for pressure changes as quickly.

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58
Q

S1

A

Atrioventricular valve closure (“Lub”)

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59
Q

S2

A

Aortic/Pulmonary valve closure (“Dub”)

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60
Q

S3

A

“Ventricular gallop” - a large amount of blood striking a stiffened left ventricle

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61
Q

S4

A

Left atrium contracts against a stiffened ventricular wall due to reduced compliance (Hypertrophy or MI)

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62
Q

Area of pressure volume loop represents…

A

Net work done

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63
Q

Ejection fraction

A

Stroke volume/End Diastolic Volume (peak volume)

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64
Q

Heart sound which corresponds with end diastolic pressure/volume

A

S1

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65
Q

Heart sound which corresponds with end systolic pressure/volume

A

S2

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66
Q

At what point in the cardiac cycle is S4 heard?

A

Just before S1, at the end of diastole

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67
Q

Factors which increase preload

A

Increased blood volume

Increased skeletal muscle pump activity

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68
Q

Factors which increase afterload

A

Hypertension
Increased peripheral resistance (atherosclerosis and arteriosclerosis
Aortic stenosis

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69
Q

Changes to pressure-volume loop as a result of increased preload

A

Taller and shifted to the right

Increased pressures and volumes generated

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70
Q

Changes in pressure-volume loop as a result of increased afterload

A

Taller

Greater pressures generated by the same volume of fluid

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71
Q

Changes in pressure-volume loop as a result of increased inotropy

A

Taller and shifted to the left

ESPVR is steeper since more pressure can be generated by a smaller volume of fluid.

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72
Q

Orthostatic Hypotension

A

Pooling of blood in veins of legs when individual changes from supine to standing.
Decrease in venous return, therefore decreased stroke volume, cardiac output and arterial pressure.
Brief moment of cerebral ischaemia before autoregulation compensates for this.

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73
Q

Baroreceptors are expressed in…

A

Carotid sinus and aortic arch walls

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74
Q

How do baroreceptors detect blood pressure?

A

Express stretch sensitive TRP family channels which are non selectively permeable to cations (Ca2+, Na+_

Increased stretching, causes increased entry of cations into afferent neurons. Many action potentials generated

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75
Q

Information from baroceptors is carried to the brain via…

A

Glossopharyngeal nerve

Vagus nerve

76
Q

Information from baroreceptors is carried to which structure in the CNS?

A

Nucleus Tractus Solitarii (NTS) in the medulla

77
Q

High blood pressure detected by baroreceptors. What is the body’s response?

A

Inhibition of sympathetic activity
Increased vagal activity

Therefore, vasodilation

78
Q

Right Vs Left sympathetic cardiac nerves

A

Right - more chronotropic (since SAN is on right)

Left - more inotropic (since muscle is thicker on left)

79
Q

Right Vs Left Vagus Nerve

A

Right - affects SAN more

Left - affects AVN more

80
Q

How does sympathetic nervous system exert its effects on blood vessels?

A

Causes vasoconstriction when noradrenaline binds to B1 receptors (Tonic constriction)

Causes vasodilation when adrenaline binds to its receptors (Preparation for fight or flight)

81
Q

How does parasympathetic nervous system exert its effects on blood vessels?

A

ACh binds to M2 receptors on smooth muscle. Results in hyperpolarisation and therefore vasodilation.

82
Q

Functional hyperaemia

A

Vasodilation in response to chemical byproducts of metabolism (CO2, K+, Lactic acid, ADP and Pi)
Facilitates removal of waste products .

83
Q

Reactive hyperaemia

A

Blood pressure is greater than normal for a brief period once pressure is relieved from an artery.
Facilitates rapid removal or waste products and supply of nutrients.

84
Q

Rate of action potential propagation in SAN

A

100bpm

85
Q

Delay if ventricular excitation due to the AVN

A

0.1s

86
Q

Bundle of His

A

Specialised large diameter cardiac myocytes arranged end to end. Excitation spreads via gap junctions.

87
Q

Effect of sympathetic stimulation on AVN

A

Shortens delay by increased permeability to Na+ - steeper pacemaker potential.

88
Q

How does sympathetic stimulation increase chronotropy?

A

Increases chance of Na+ channels opening - steeper pacemaker potential (phase 4), shorter distance between peaks

89
Q

How does parasympathetic stimulation decrease chronotropy?

A

Increases chance of K+ channels opening - hyperpolarisation at the end of phase 3, takes longer for membrane potential to reach threshold level, longer distance between peaks.

90
Q

Phase 4 of pacemaker potential

A

Na+ entry into pacemaker cell

91
Q

Phase 0 of pacemaker potential

A

Rapid influx of Ca2+ into pacemaker cell

92
Q

Phase 1 of pacemaker potential

A

Does not exist

93
Q

Phase 2 of pacemaker potential

A

Does not exist

94
Q

Phase 3 of pacemaker potential

A

K+ efflux from pacemaker cell

95
Q

Phase 4 of myocyte action potential

A

Na+ and Cl+ leaking into myocyte - increasing membrane potential from -90 to -70mV

96
Q

Phase 0 of myocyte action potential

A

At -70mV (threshold), Na+ channels open and flood into cell causing depolarisation up to 20mV

97
Q

Phase 1 of myocyte action potential

A

At 20mV, Na+ channels close, membrane potential begins to fall since K+ is the dominant ion

98
Q

Phase 2 of myocyte action potential

A

Membrane potential has reached 5mV due to outward movement of K+ in phase 1. At 5mV, Ca2+ channels open.
Membrane potential remains constant since outward K+ is balanced by Ca2+ in

99
Q

Phase 3 of myocyte action potential

A

Spontaneous closure of Ca2+ channels. Membrane potential returns to -90mV since K+ is the dominant ion.

100
Q

Effect of sympathetic stimulation on myocyte action potential

A

Activation of PKA (Binding of catecholamines to B1 adrenoceptors) which phosphorylates delayed rectifier K+ channels. Increases rate at which ventricular myocytes repolarise.

101
Q

In a heart transplant patient, there is no autonomic innervation of the heart. How can heart rate be increased in response to exercise?

A

Increased venous return due to skeletal muscle pump.
Frank Starling mechanism states that the heart must pump out of the right atrium all the blood returned to it without letting any back up in the veins.

102
Q

How do catecholamines cause an increased inotropy?

A

Noradrenaline/Adrenaline bind to B1 adrenoceptors.
Activates AC, increasing cAMP, activation of PKA.
PKA phosphorylates L-type Ca2+ channels, causing them to open.
Greater influx of Ca2+ therefore increased strength of contraction.

103
Q

How do caffeine and theophylline cause an increase in chronotrophy and inotropy?

A

Inhibit phosphodiesterase which normally breaks down cAMP.

Therefore, increased [cAMP]

104
Q

What is the difference between the effects of alpha and beta adrenoceptor activation on blood vessels?

A

Alpha - vasoconstriction (normally noradrenaline acts on this)
Beta - vasodilation (normally adrenaline acts on this)

105
Q

Effect of vasopressin/ADH on blood vessels

A

Vasoconstriction in most tissues
Vasodilation in cerebral and coronary vessels

(Released in response to substantial haemorrhage)

106
Q

Coronary blood flow throughout the cardiac cycle

A

Increased coronary blood flow during diastole due to extravascular compression during systole (endocardial vessels affected more than epicardial)

107
Q

Thebesian Veins

A

Minute, valveless venous channels that open directly into the chambers of the heart from the capillary bed in the cardiac wall.
Enables collateral circulation (unique to the heart)

108
Q

Compensatory mechanism which ensures adequate coronary blood flow during sympathetic stimulation

A

Sympathetic stimulation causes vasoconstriction of coronary vessels BUT accumulation of metabolites causes vasodilation (stronger effect than SNS)

109
Q

Metabolic regulation of vasodilation/vasoconstriction

A

Low O2, high CO2 and H+ cause VASODILATION (inhibition of Ca2+ entry to smooth muscle cells)

High K+ causes VASODILATION (inhibition of Ca2+ entry into smooth muscle cells)

110
Q

Effect of adenosine on blood vessels

A

Vasodilation

111
Q

Why does cardiac ischaemia cause pain?

A

Oxygenated blood supply cannot meet myocardial demand. Anaerobic respiration by myocytes generates lactate.
Build up of lactic acid and low pH causes PAIN.

112
Q

How does digoxin increase inotropy?

A

Inhibits Na+(out)/K+(in) ATPase
Increased [Na+] intracellularly

Na+(in)/Ca2+(out) exchange cannot occur.
Increased [Ca2+] intracellularly

Stimulates calcium induced calcium release from sarcoplasmic reticulum
Therefore, contraction is stronger

113
Q

Effect of digoxin on chronotropy and dromotropy

A

Parasympathomimmetic - negative chronotrope and dromotrope

114
Q

Stable Angina

A

Crushing, burning or tight pain in the chest precipitated by physical exertion or emotional stress.
Often accompanied by dyspnoea, nausea, sweating
Relieved by rest

AKA Classical/Exertional angina

115
Q

Decubitus Angina

A

Occurs when patient lies down.

Usually associated with heart failure - due to increased central blood volume and consequent myocardial tensions.
Often have Coronary artery disease

116
Q

Nocturnal angina

A

Wakes a person from sleep, triggered by vivid dreams.

Usually have critical coronary artery disease and may be associated with vasospasm

117
Q

Variant angina

A

No provocation, occurs at rest, at night or early in the morning.
Prolonged and more severe pain.
Affects women more often than men
Caused by coronary artery spasm

118
Q

Risk factors for angina

A 
Obesity 
Family History
Smoking 
Kidney disease
Physical inactivity
Hypercholesterolaemia
HTN
Diabetes
Age (F >65, M>55)
Psychosocial stress
119
Q

ECG changes in angina

A

ST depression due to cardiac ischaemia

120
Q

Imaging techniques used in diagnosis of angina

A

Coronary angiography - X ray based imaging, identifies narrowing of coronary arteries (injection of radio-opaque contrast dye into coronary arteries)

Echcardiography - Non invasive US imaging, identifies chamber wall abnormalities

121
Q

First line treatment of Angina

A

Beta blocker or calcium channel blocker - depending on comorbidities

If ineffective, try the other option or both.

122
Q

Second line treatment of Angina

A

If beta blocker and calcium channel blocker are not tolerated or both are contraindicated.
Try one of the following:
Long acting nitrate, ivabradine, nicorandil, ranolazine

123
Q

Calcium channel blockers used to treat angina

A

Diltiazem

Verapamil

124
Q

Important ADRs of CCBs

A

Heart block
Negative inotropy
Constipation

125
Q

MOA of Nicorandil

A

Katp channel activation (hyperpolarisation, preventing Ca2+ entry) and NO donor

126
Q

ADRs of nicorandil

A

Rectal bleeding and flushing

127
Q

MOA of Ivabradine

A

Sinus node Kf channel blocker (Rate limiter)

128
Q

ADRs of Ivabradine

A

Bradycardia
Heart failure
AF

129
Q

MOA of Ranolazine

A

Uncertain

Na+ channel blocker and myocyte metabolic substrate utilisation

130
Q

ADRs of Ranolazine

A

QT prolongation

131
Q

Exogenous NO donors used in the treatment of Angina

A

Glyceryl trinatrate sublingual spray

Isosorbide trinitrate

132
Q

ADRs of GTN spray

A

Headache
Postural hypotension
Rapid intolerance (4-12hrs nitrate-free period required daily to prevent loss of efficacy)

133
Q

How does sympathetic stimulation increase lusitropy?

A

Activated PKA phosphorylates phospholamban.
Phosphorylated phospholamban has no inhibitory effect on RyR receptor therefore Ca2+ reuptake is faster.
Increased rate of relaxation.

134
Q

Elastic arteries:

A

Aorta and pulmonary artery

135
Q

Discontinuous capillaries are only found in…

A

The liver - between sinusoids and hepatocytes

136
Q

Endothelium which lines the inner surface of blood vessels

A

Simple squamous (tunica intima)

137
Q

Connective tissue which makes up the epicardium

A

Adventitia

138
Q

Intercalated discs

A

Region where ends of cardiac myocytes are connected.
Contains gap junctions, adherens junctions and desmosomes.
Gap junctions allow for electrical coupling

139
Q

Pericardium

A

2 layers connective tissue sac that encloses the heart.

Fibrous and a serous layer. Serous secretes serous fluid.

140
Q

Endocardium

A

Lining of chambers and covering of heart valves.

Consists of endothelium, basement membrane and a small layer of loose connective tissue and some adipose tissue

141
Q

Functions of pericardium

A

Protects against overfilling
Mechanical protection
Holds the heart in place
Protects heart from infection from other organs

142
Q

Referred Pain

A

General visceral afferent (GVA) pain fibers follow sympathetic fibers back to the same spinal cord segments that gave rise to the preganglionic sympathetic fibers.

143
Q

Symptoms of Pericarditis

A

Flu-like (night sweats, malaise, fever)
Dyspnoea
Chest pain (sharp, when lying down or bending, with deep inspiration and with pulsation of heart)

144
Q

Pain sensation in pericarditis

A

Sensation comes from parietal layer due to afferent fibres which transmit sensation through the PHRENIC nerve (C3,4,5).

Caused by friction rub or effusion.

Pain may be visceral or referred (supraclavicular region).

145
Q

Acute idiopathic pericarditis tends to occur in…

A

Young adults

146
Q

Causes of pericarditis

A 
Physical trauma/irradiation
Haemorrhage (trauma/aortic rupture)
Neoplasia
Systemic disorders i.e. CT disease 
Infective 
Acute idiopathic
147
Q

Pericarditis on an ECG

A

Stage I - ST elevation and PR depression in I, II, aVL, aVF, V2-6. Reciprocal ST depression and PR elevation in aVR.

Stage 2 - normalisation of ST. Generalised T wave flattening

Stage 3 - Inversion of T waves (3+ wks)

Stage 4 - Normal ECG (several wks)

148
Q

Investigations in diagnosis of pericarditis

A

Pericardial paracentesis

Echocardiogram

149
Q

Why is pain in pericardium relieved by sitting up and bending forward?

A

Pulls diaphragm down, creating more space between parietal and visceral pericardium. Reduced friction between them.

150
Q

Symptoms of aortic dissection

A 
Severe chest pain
Sudden onset 
Radiation to neck and back
Autonomic symptoms: N+V, sweating, fainting, hiccups 
Numbness in limbs
151
Q

Type I DeBakey Classification

A

Aortic dissection involving the ascending aorta, aortic arch and descending aorta

152
Q

Type II DeBakey Classification

A

Aortic dissection involving ascending aorta only

153
Q

Type III Debakey Classification

A

Aortic dissection confined to descending aorta, distal to left subclavian.

Type A - Extending proximally and distally, mostly above diaphragm

Type B - Extending only distally, mostly below diaphragm

154
Q

Symptoms specific to proximal aortic dissection

A

Anterior chest pain

155
Q

Symptoms specific to distal aortic dissection

A

Interscapular and back pain

156
Q

Factors which increase risk of Aortic Dissection

A 
HTN
Marfan's Syndrome
Bicuspid aortic valve 
Coarctation (narrowing) of aorta 
Pregnancy
Ehlers-Danlos Syndrome
157
Q

Marfan’s Syndrome

A

Genetic connective tissue disorder.

Extremely tall, have long slender fingers and toes, partial dislocation of lens and heart defects.

158
Q

Ehlers-Danlos Syndrome

A 
Abnormal or deficient collagen 
Have elastic, fragile skin
Easily bruised 
Scars poorly 
Hypermobility - joints easily dislocate
Weaker heart valves
159
Q

Management of Aortic Dissection

A

Emergency cardiac surgery
Treatment of risk factors (usually HTN)
Treat severe pain

160
Q

Most effective treatment of nicotine dependence

A

Nicotine replacement therapy by patch and inhaler (31.5%)

161
Q

How can pericardial effusion be differentiated from cardiac tamponade?

A

Both involve build up of fluid in pericardium.
Tamponade has more severe symptoms: dyspnoea, hypotension, distant heart sounds. Pericardial effusion may be asymptomatic or experience chest pain/pressure.

162
Q

Site of auscultation of aortic valve

A

2nd intercostal space, right sternal border

163
Q

Site of auscultation of pulmonary valve

A

2nd intercostal space, left sternal border

164
Q

Site of auscultation of Tricuspid Valve

A

5th intercostal space, left sternal border

165
Q

Site of auscultation of Mitral valve

A

5th intercostal space, left midclavicular line

166
Q

Ligamentum arteriosum

A

Remnant of Ductus Arteriosum which connects pulmonary artery to proximal descending aorta in the foetus (allowing blood to bypass non functioning fluid filled lungs).

167
Q

Surgical treatment for angina

A

Coronary artery bypass - improves blood supply to myocardium.

168
Q

Why might a patient opt for a biological mitral valve replacement over a mechanical one?

A

Mechanical valves require lifelong treatment with warfarin which cannot be taken when pregnant or if patient is active and at risk of injury.
Therefore younger patients will opt for biological valve.

Biological valves will only last 12-15yrs, whereas mechanical valves are lifelong.

169
Q

Troponin as a cardiac biomarker

A

Cardiac specific - released in myocardial injury (undetectable in health).

Not released instantly, therefore troponin must be taken 12 hrs later and compared with first sample.

170
Q

Parenteral Anticoagulants

A

Heparin (IV)
LMWH - Enoxaparin (SC)
Fondaparinux (SC)

171
Q

ADRs of parental anticoagulants

A

Bleeding
Purpura (purple toes)
Heparin induced thrombocytopenia.

172
Q

MOA of warfarin

A

Vitamin K epoxide reductase shuttle inhibition.

Inhibition of synthesis of factors II, VII, IX and X

173
Q

ADRs of oral anticoagulants

A

Haemorrhage
Purpura (purple toes)
Skin necrosis

174
Q

Antiplatelet drugs

A

Aspirin

Clopidogrel

175
Q

MOA of Aspirin

A

Irreversible inhibition of COX enzyme. Suppression of PG and thromboxane synthesis therefore reduced platelet aggregation

176
Q

ADRs of Aspirin

A 
GI irritation and ulceration
Bleeding
Nephrotoxicity 
HTN
Reye's Syndrome (if given to under 16s, unless for Kawasaki Disease)
177
Q

MOA of clopidogrel

A

Pro drug, its active metabolite reduces platelet aggregation through inhibition of ADP-dependent activation of the GPIIb/IIIa receptor (P2Y12 ADP receptor inhibitor)

178
Q

ADRs of clopidogrel

A

Dyspepsia
Bleeding
Diarrhoea
Abdominal pain

179
Q

Indication for aspirin

A

Secondary prevention in CVD
TIA
Acute stroke (for 14 days)
Acute coronary syndrome

180
Q

Indication for clopidogrel

A

NSTEMI

Stroke (after 14 days of aspirin)

181
Q

ADRs of warfarin

A

Haemorrhage
Hepatic Dysfunction
Jaundice
Nausea

182
Q

Contraindications of warfarin

A

Harmorrhagic cardiovascular accident
Excessive bleeding
INR>4.5

183
Q

Contraindications of Clopidogrel

A

Active bleeding

Prior to elective surgery

184
Q

MOA of Tenectaplase

A

Fibrinolytic - a recombinant form of tPA which mediates conversion of plasminogen to plasmin.
More plasmin which rapidly dissolves clots by causing fibrinolysis

185
Q

ADRs of Tenectaplase

A 
Serious bleeds
Reperfusion pathologies (cerebral oedema)
186
Q

Contraindications of Tenectaplase

A

Recent haemorrhage On anticoagulant or antiplatelet drugs
Aneurysm
Aortic dissection

Year 2 (17 decks)

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