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phase 2 > Cardio > Flashcards

Cardio Flashcards

1
Q

Atherosclerosis is a primary cause of which three diseases

A

Heart attack, stroke and gangrene of the extremities

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2
Q

What affects the distribution of atherosclerotic plaques

A

Haemodynamics (flow and turbulence) cause media thinning and altered gene expression

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3
Q

Angina pectoris

A

Pain in the centre of the chest which is brought on by exercise and relieved by rest, may spread to the jaw and arms. Caused by increased myocardium oxygen demand and insufficient supply by the coronary arteries. Almost exclusively secondary to atherosclerosis

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4
Q

What is the response to injury hypothesis

A

Atherosclerosis is initiated by injury to endothelial cells leading to endothelial dysfunction, leukocyte accumulation and migration

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5
Q

What is ischaemia-reperfusion injury

A

Reintroduction of blood flow following ischaemia causes oxidative stress and neutrophils migrate causing inflammation and further damage to the tissue

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6
Q

Name some examples of good inflammation

A

Pathogens, parasites, tumours and wound healing

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7
Q

Name some examples of bad inflammation

A

Myocardial reperfusion injury, IHD, atherosclerosis, Rheumatoid arthritis and asthma

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8
Q

What are the two factors which ignite inflammation in the arterial wall

A

LDL and endothelial dysfunction

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9
Q

Which inflammatory cytokines are found in plaques

A

IL-1, IL-6, IL-8, INF-gamma, TGF-beta, MCP-1

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10
Q

What are foam cells

A

Lipid laden macrophages

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11
Q

What are the two types of coronary arteries

A

Epicardial (Run along surface of the heart, LAD, RCA, Cx) and small vessels (run within the cardium)

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12
Q

What are causes of angina

A

Atherosclerosis, anaemia, obstruction of vessels (ie from LV hypertrophy) increasing distal resistance

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13
Q

Name three other causes of angina besides atherosclerosis

A

Prinzmetals (coronary spasm), Syndrome X (microvascular resistance), Crescendo and unstable angina: ACS

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14
Q

What are the 3 factors needed for angina pain

A

heavy central tight radiates, exertion preciptitates, relieved by rest/GTN

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15
Q

Angina differential diagnosis

A

Pericarditis, PE, Chest infection, Aortic dissection, GI, MSK, psychological

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16
Q

Signs of complications on examination

A

Scars (midline sternonotomy, pacemaker, legs)

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17
Q

What is a sign unique to angina

A

Leivens sign, where they clutch hand across chest

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18
Q

What are the signs of angina on ECG and Echo

A

There are no direct signs. Can show IHD or previous infarcts

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19
Q

What are the signs of IHD and previous infarcts on ECG and Echo

A

Q waves, T wave inversion and BBB

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20
Q

What sign on an ECG during exertion indicates ischaemia

A

ST depression

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21
Q

Name two beta 1 specific beta blockers

A

Atenolol and bisoprolol

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22
Q

Beta blocker side effects

A

Tiredness, nightmares, bradycardia, cold hands and feet, erectile dysfunction

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23
Q

Beta blocker contraindications

A

Asthma, excess bradycardia, heart block, prinzmetal’s angina

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24
Q

How do nitrates treat angina

A

As venodilators they reduce the preload, work and oxygen demand of the heart. They also dilate the coronary arteries.

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25
Q

How do CCBs treat angina

A

As arterodilators they reduce the afterload, work and oxygen demand of the heart. They also dilate the coronary arteries and are negatively ionotropic

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26
Q

Is a CABG or PCI used in STEMI

A

Definitely PCI

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27
Q

Is a CABG or PCI used in NSTEMI

A

CABG can be used but PCI preferred

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28
Q

CABG or PCI in stable angina

A

Either. CABG more invasive but better prognosis and for complex disease

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29
Q

What is the J point on the ECG

A

Point of inflection between QRS complex and T wave (end of s wave, start of ST segment)

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30
Q

What difference is needed to consider it elevation or depression

A

One box

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31
Q

What are Q waves caused by

A

Absence of electrical activity due to scar tissue, therefore a sign of previous infarction

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32
Q

Name the features of a non Q wave MI

A

Poor R wave progression, ST elevation and biphasic T wave

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33
Q

Features of a Q wave MI

A

No R wave, too late to treat

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34
Q

What is the primary cause of ACS

A

Atherosclerotic plaque rupture and subsequent thrombosis

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35
Q

In which groups are silent ACS more commonly seen

A

The elderly and diabetic

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36
Q

Name some lesson common causes of ACS

A

Coronary vasospasm, aortic dissection, drug abuse and coronary artery dissection due to defects of vessel connective tissue

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37
Q

What are the signs of heart failure

A

Raised JVP, 3rd Heart Sound and basal crepitations

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38
Q

What is a pansystolic murmur a sign of

A

Papillary muscle dysfunction/rupture or VSD

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39
Q

Which two molecules are most associated with cardiac muscle damage

A

Troponin I and T

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40
Q

How do troponin levels differ in ACS vs other cardiac conditions

A

Big changes hour to hour, peaking at two hours. Whereas in non ACS there is ongoing damage so little change

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41
Q

How does aspririn work

A

It irreversibly inhibits COX (thromboxane synthetase), reducing the production of the pro-aggregatory factor thromboxane from arachidonic acid

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42
Q

Why is aspirin effective at low doses

A

As platelets just have a short life time and are anucleate so unable to produce more COX, the effects therefore only wear off as new platelets are made

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43
Q

What is the purpose of platelet alpha granules secretion

A

Coagulation and inflammation

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44
Q

What is the purpose platelet dense granules secretion

A

Contribute to platelet activation

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45
Q

What catalyses the conversion of plasminogen to plasmin

A

tPA

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46
Q

What catalyses the conversion of fibrin to FDP

A

Plasmin

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47
Q

Name a P2Y12 antagonist and its effects

A

Clopidogrel reduces amplification of platelet activation

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48
Q

Name a GPIIb/IIIa antagonist and its effects

A

abciximab, prevents platelet aggregation

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49
Q

What delays the absorption of some antiplatelet drugs

A

Opiates like morphine

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50
Q

Which anticoagulant is used in NSTE ACS

A

Fondaparinux, a low level anticoagulant

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51
Q

What is the initial pain relief used in ACS

A

Morphine+Metaclopramide, nitrates

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52
Q

What is the antianginal pharmacological therapy

A

Beta blockers, nitrates, calcium channel blockers

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53
Q

What is the secondary prevention in ACS pharmacological therapy

A

Statins, ACE inhibitors, Beta Blockers or other antihypertensives

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54
Q

What is the pharmacological therapy in heart failure patietns

A

Diuretic, ACEI, Beta blocker, aldosterone antagonist

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55
Q

Name an aldosterone antagonist

A

Spironolactone

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56
Q

What is the treatment of acute STEMI when PCI is not available

A

Fibrinolytic intervention

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57
Q

What is tako-tsubo

A

Stress induced cardiomyopathy

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58
Q

Factors affecting response to clopidogrel

A

Dose, age, weight, DM or CKD, Cytochrome P450 inhibitors or dysfunction

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59
Q

How does tricagelor work

A

Reversible P2Y12 inhibitor and inhibits adenosine uptake in the ENT pathway

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60
Q

What are common P2Y12 inhibitor side effects

A

Bleeding, rash, GI disturbance

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61
Q

When are nitrates given in ACS

A

Unstable angina and coronary vasospasm

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62
Q

Define ECG

A

Representation of the electrical events of the cardiac cycle

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63
Q

What is the intrinsic rate of the SA node

A

60-100bpm

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64
Q

What is the intrinsic rate of the AVN

A

40-60bpm

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65
Q

What is the intrinsic rate of ventricular cells

A

20-45bpm

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66
Q

Define syncope

A

Temporary loss of consciousness due to insufficient blood supply to the brain

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67
Q

What is the standard calibration of ECG

A

25mm/s 0.1mV/mm

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68
Q

What does the P wave represent

A

Atrial depolarisation

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69
Q

What does the QRS complex represent

A

Ventricular depolarisation

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70
Q

What does the T wave represent

A

Ventricular repolarisation

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71
Q

What is the PR interval

A

The time taken for atrial depolarisation and delay in the AV junction (AV node and bundle of his) - start of P till QRS

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72
Q

What are PR segment abnormalities associated with

A

Pericarditis or atrial ischaemia

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73
Q

What is the PR segment

A

End of P till QRS

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74
Q

What are ECG leads

A

Leads which measure the electrical potential between two points

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75
Q

Whats the difference between bipolar and unipolar leads

A

Bipolar leads= two different points on the body, Unipolar leads= one point on the body and a virtual reference point with 0 electrical potential in the centre of the heart

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76
Q

What is lead 1

A

Right to left shoulder 0 degrees

77
Q

What is lead 2

A

right arm to left leg, pointing down 60 degrees

78
Q

What is lead 3

A

Left arm to left leg, 120 degrees

79
Q

What is aVR

A

Augmented vector right, shoulder -150 degrees

80
Q

What is aVL

A

Augmented vector left, shoulder -30 degrees

81
Q

What is aVF

A

Augmented vector foot, pubic symphsis 90 degrees

82
Q

What does the QRS complexes in leads I and II pointing away from each other represent

A

Lovers Leaving, Left axis deviation

83
Q

What does the QRS complexes in leads I and II +- III pointing towards each other represent

A

Lovers returning, Right axis deviation

84
Q

Where is lead 1

A

Information between aVL and a VR

85
Q

Where is lead 2

A

Information between aVL and aVF

86
Q

Where is lead 3

A

Information between aVF and aVR

87
Q

V1 position

A

4th intercostal space, right border of the sternum

88
Q

V2 position

A

4th intercostal space, left border of the sternum

89
Q

V3 position

A

Midway between the placement of leads V2 and V4

90
Q

V4 position

A

5th intercostal space, midclavicular line

91
Q

V5 position

A

Anterior axillary line on same horizontal level as V4

92
Q

V6 position

A

Midclavicular line on same horizontal level as V4,5,6

93
Q

Which ECG leads represent the lateral heart territory and which coronary artery supplies this

A

I, aVL, V4-6 Circumflex

94
Q

Which ECG leads represent the anterioseptal heart territory and which coronary artery supplies this

A

V1-3 LAD

95
Q

Which ECG leads represent the inferior heart territory and which coronary artery supplies this

A

2,3,aVF (VF=2 AND 3 LINES), RCA (80%) Cx (20%)

96
Q

Which ECG leads represent the posterior territory and which coronary artery supplies this

A

V7-9 and Cx

97
Q

What can a tall pointed P wave suggest

A

Right atrial hypertrophy or high atrial pressure, such as in COPD ‘p pulmonale’

98
Q

What can a notched P wave in limb leads suggest

A

Left atrial problem eg mitral valve disease ‘p mitrale’

99
Q

What is the R wave

A

The first positive deflection in the QRS complex

100
Q

What is the Q wave

A

The first negative deflection in the QRS complex

101
Q

What is the QT interval for a heart rate of 70bpm

A

Less than 0.40s

102
Q

What factors increase the chance of seeing U waves

A

Bradykinia or hypothermia or slow heart rate

103
Q

What is the rule of 300

A

300/big boxes between two QRS is the bpm

104
Q

What does the QRS axis represent

A

Overall direction of the heart’s electrical activity

105
Q

What is the normal axis

A

-30 to +90 degrees

106
Q

What is a left axis deviation

A

-30 to -90 degrees

107
Q

What is a right axis deviation

A

+90 to +180 degrees

108
Q

In which direction does the IV septum depolarise

A

Left to right

109
Q

Name causes of hypertension

A

85% aetiology unknown, 15% aldosterone overproduction 5% other inc renal failure, drugs and hormone secreting tumours

110
Q

What is Conns syndrome

A

Overproduction of aldosterone due to a unilateral adrenal adenoma which causes sodium and fluid retention

111
Q

Which drugs cause HTN

A

NSAIDS, combined oral contraceptives, corticosteroids, ciclosporins, cold cures, SRNI antidepressants, some recreational drugs such as cocaine and amphetamine

112
Q

What is malignant hypertension

A

Rapid rise in HTN, untreated=dead within 6 months, causes immediate damage to small blood vessels in kidneys and eyes, look to the eyes to check

113
Q

What is phaechromacytoma

A

Rare adrenal tumour causing excessive adrenaline and noradrenaline production

114
Q

How does angiotensin cause HTN

A

Causes vascular growth, salt retention and increased peripheral resistance

115
Q

How are RAAS linked

A

Sympathetic stimuli can cause renin release from kidney and Angiotensin II can cause noradrenaline release

116
Q

Name an ACE inhibitor and how they work

A

Ramipril, Less Angiotensin II and therefore less vasoconstriction and aldosterone. Reducing PVR and therefore afterload and BP. Reducing fluid retention (less aldosterone and increased efferent arteriole pressure) and therefore preload, helping heart failure.

117
Q

What is the effect of ACE-inhibitors on bradykinin production

A

Less conversion to inactive peptides. More bradykinin can lead to dry cough (10%), rash and anaphylactoid reactions

118
Q

ACE inhibitors are most effective in which groups

A

Young people

119
Q

When would an ARB be used in hear failure

A

When ACE-I is contraindicated, perhaps because of the dry cough caused by bradykinin

120
Q

Name an ARB and how they work

A

Candesartan, blocks the peripheral angiotensin II receptor. AT-1

121
Q

Name a CCB and how they work

A

Amlodidpine, inhibit voltage gated L-type calcium channels in vascular smooth muscle, reducing vasoconstriction

122
Q

What are adverse effects from peripheral vasodilation

A

Flushing, headache, oedema and palpitations

123
Q

What are adverse effects from negatively chronotropic agents

A

Bradycardia and AV block

124
Q

What are the adverse effects from negatively ionotropic agents

A

Worsening heart failure

125
Q

What is verapamil and an adverse effect

A

Phenylalkylamine CCB with negative chrono and ionotropic effects on the heart causes constipation

126
Q

Name a BB and how they work

A

Metoprolol, targets B1 and reduces the chronotropic and ionotropic activity of the heart, prolongs AV node refractory period and reduces renin secretion

127
Q

Which B receptors are found in the heart

A

60% B1, 40% B2

128
Q

Which are the more B1 selective beta blockers

A

Metropolol and bisoprolol

129
Q

What do thiazide diuretics target and an example

A

Sodium reabsorption via luminal Na/Cl cotransporter in the DCT, bendroflumethiazide

130
Q

What do loop diuretics target and an example

A

NaKCC cotransporters in the thick arm of the loop of henle, Furosemide

131
Q

What do K+ sparing diuretics target and an example

A

Competitively binds to aldosterone receptors, on ENaC in DCT, sprionalactone

132
Q

Loop diuretics main adverse effects

A

Hypovolaemia and hypotension, low electrolytes raised urea

133
Q

Name an alpha 1 adrenoceptor blocker

A

Doxazosin

134
Q

Name a centrally acting antihypertensive

A

Methyldopa

135
Q

Name a direct renin inhibitor

A

Aliskiren

136
Q

What is step 1 in HTN treatment

A

Under 55: ACE-I/ARB

Over 55 or afrocarribean: CCB

137
Q

What is step 2 in HTN treatment

A

ACE-I/ARB and CCB

138
Q

What is step 3 in HTN treatment

A

ACE-I/ARB and CCB and thiazide like diuretic

139
Q

What is step 4 in HTN treatment

A

This is resistant HTN, consider higher dose thiazide, spironolactone, alpha or beta blocker

140
Q

What drop would you expect after atenolol treatment

A

-10/-5

141
Q

Define heart failure

A

An inability of the heart to deliver blood and oxygen at a rate commensurate with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures (Cardiac output is inadequate for the body’s requirements)

142
Q

What is the most common cause of heart failure

A

Myocardial dysfunction from IHD

143
Q

What is ADCHF and who gets it

A

Acute decompensated CHF with reduced ejection fraction (<40%), generally younger than 70 and male(IHD)

144
Q

What are the three cardinal symptoms of HF and the two more specific symptoms

A

SOB, ankle oedoma and fatigue. Orthopnoea and paroxysmal episodic nocturnal breathing

145
Q

What is orthopnoea

A

Breathlessness which prevents the patient lying down, they must be sitting up/standing

146
Q

Causes of acute decompensation of chronic heart failure

A

Negative ionotropes, AMI, HTN, Obesity+Alcohol, super infection, AF and arrythmias, non compliance, NSAIDS

147
Q

Complications of heart failure

A

Renal dysfunction, Rhythm disturbances, systemic thromboembolism, DVT and PE, LBBB and bradycardia, hepatic and neurological dysfunction

148
Q

What is the role of ANP (atrial) and BNP (ventricular)

A

Assist the stretched atria by increasing the GFR and reducing sodium resorption, reducing fluid load, smooth muscle stretch and preload

149
Q

What is the effect of AT 1 receptor activation

A

Vasoconstriction, water and salt retention

150
Q

What is the effect of AT2 receptor activation

A

Vasodilation and antiproliferation with kinins

151
Q

Name a pottasium sparing diuretic

A

Spironolactone, an aldosterone antagonist

152
Q

What are hydralazine and nitrates

A

Vasodilators

153
Q

What is digoxin

A

An ionotrope

154
Q

Which races dont ACE-I work in

A

Afrocarribean - equatorial

155
Q

Which 4 BB are aloud in those with HF

A

Bisoprolol, metrapolol, nivedrolol, calvetolol

156
Q

What treatment is used in congestive heart failure with preserved ejection fraction

A

Diuretics

157
Q

Which treatment doesnt work in AF

A

Beta blockers

158
Q

Cardiac resynchronisation therapy

A

pace right ventricle, atrium and coronary sinus artery to left ventricle wall. This can resync heart and reduce mortality

159
Q

Name some care issues in those with congenital heart problems

A

Intellectual disability, psychosocial issues, transition, explaining the lesion and prognosis, building independence/self reliance

160
Q

What should be advised against in those with congenital heart defects

A

Pregnancy, heart cant tolerate extra strain

161
Q

What are the four features of tetralogy of fallot

A

Ventricular septal defect, pulmonary stenosis, hypertrophy of right ventricle and overiding aorta

162
Q

What is normal pulmonary pressure

A

30/10

163
Q

What causes cyanosis

A

Desaturation of haemoglobin due to reduced oxygen levels or septal defects leading to mixing of blood

164
Q

What does thrill as a clinical sign mean

A

buzzing sensation

165
Q

What are the clinical signs of a large VSD

A

Small breathless skinny baby, increased heart size, rate and respiratory rate. Murmur varies in intensity

166
Q

What are the clinical signs of a small VSD

A

Fully grown, normally asymptomatic with normal HR, RR and heart sound but can a loud systolic heart murmur and thrill

167
Q

What direction does the cardiac shunt have to be to get cyanosis

A

Right to Left (unusual as Right normally lower pressure)

168
Q

What are the clinical signs of ASD

A

Pulmonary flow murmur, fixed split second heart sound, big pulmonary arteries and heart on CXR

169
Q

What is a primum ASD

A

Defect associated with AV valve abnormality

170
Q

What is secondum ASD

A

Defect associated with a hole high in septum

171
Q

What is sinus venosus ASD

A

Patent sinus venosus from development, leads to SVC entry into right atrium

172
Q

What is AVSD and which condition is it associated with

A

Hole in heart, chambers and valves havent met in complete. Associated with Downs

173
Q

When are ASD and AVSD operated on

A

When there is right heart dilatation

174
Q

How do you differentially diagnose patent ductus arteriosus from eisenmengers

A

Both with have blue clubbed toes, but patent ductus arteriosus will have pink unclubbed fingers

175
Q

What are the clinical signs of patent ductus arteriosus

A

Continous machinery murmur, if large big heart and breathless

176
Q

What is coarctation of the aorta

A

Narrowing of the aorta at the site of insertion of the ductus arteriosus

177
Q

What is a bruit

A

A murmur heard over a vessel with turbulent flow, commonly caused by narrowing of an artery

178
Q

Clinical signs of coartctation of the aorta

A

Right arm HTN, murmur, bruits over scapulae and back from collateral vessels

179
Q

What causes HTN in coarctation of the aorta

A

Reduced blood flow to the kidneys leads to increased blood pressure in the right arm, head and neck

180
Q

Define pulmonary stenosis

A

Narrowing of the outflow tract of the right ventricle

181
Q

What are the two valvular defects which cause murmur

A

Aortic stenosis and mitral regurgitation (ASMR)

182
Q

What is the fontan procedure

A

Where a one ventricle circulation is formed

183
Q

When does the glenn procedure do

A

Plugs the SVC into pulmonary artery

184
Q

What does a fixed split second heart sound, sound like

A

Lub dub dub

185
Q

What are percutaneous operations

A

Where it is done through needle puncture to the skin

186
Q

Angioplasty meaning

A

Surgical repair or unblocking of an artery

187
Q

Define syncope

A

(fainting), loss of consciousness due to a sudden drop in blood pressure, resulting in a temporarily insufficient flow of blood to the brain

188
Q

Name causes of syncope

A

Vasovagal, situation and carotid sinus syncope; stokes-adams attacks (hypoglycaemia, orthostatic hypotension and anxiety)

phase 2 (17 decks)

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