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Fifth Year Medicine > Cardio > Flashcards

Cardio Flashcards

1
Q

Which cause of cardiac pain improves on leaning forwards?

A

Pericarditis

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2
Q

What conditions may cause angina?

A

Coronary artery disease
Aortic stenosis
Hypertrophic cardiomyopathy
Paroxysmal supraventricular tachycardia

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3
Q

Examination finds shock with raised JVP. Diagnosis?

A

Cardiac tamponade

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4
Q

Simple bedside test to look for aortic dissection?

A

unequal BP in both arms

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5
Q

On ECGs which features make a Q wave ‘pathological’ ?

What do they indicate?

A

Deeper than 2mm
Especially in R-sided leads V1-V3

Prior or current MI

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6
Q

What is the different pattern expected in ST depression caused by ischaemia Vs digoxin?

A 
Digoxin = downward sloping
Ischaemic = horizontal
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7
Q

Which ECG leads reflect the inferior aspect of the heart?

A

II, III, aVF

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8
Q

Which aspect of the heart do the following ECG leads indicate: V1-V4?

A

Anteroseptal

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9
Q

Which are the anterolateral leads of the heart?

A

V5-V6, I, aVL

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10
Q

Which leads are affected in a posterior MI?

A

Tall R and ST depression in V1-V2

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11
Q

MI in anteroseptal leads suggests which artery is affected?

A

Left anterior descending

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12
Q

Which artery of the heart is likely to be implicated in inferior MIs?

A

Right coronary

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13
Q

Which artery of the heart is likely to be implicated in posterior MIs?

A

Circumflex

Or right coronary

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14
Q

What adjuncts are available to help patients stop smoking?

A

Nicotine gum
Nicotine patches
Varenicline- selective nicotine R partial agonist
Bupropion- acts on noradrenaline and dopamine and nicotine systems

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15
Q

On the ECG there are tall tented T waves and absent P waves. What is the likely cause?

A

Hyperkalaemia-
T waves are from repolarisation, if the extracellular levels of K+ are high then the inside of cardiac cells is relatively more negative, so a greater change in charge occurs (resting potential is more negative + cells are less excitable)

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16
Q

What change on the ECG is seen in hypercalcaemia?

A

Short QT interval
High levels of Ca increase the speed of the plateau phase of the action potential (many channels are voltage gated so the faster a voltage is reached the quicker the cycle)

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17
Q

Causes of right bundle branch block?

A

Due to R-ventricular strain, slowing the QRS complex

Normal variant
Pulmonary embolism
Cor pulmonale (R-ventricular strain secondary to pulmonary hypertension)
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18
Q

Rx for acute heart failure with systolic dysfunction (echo shows reduced left ventricular ejection fraction)?

What additional medication can be given if systolic BP is below 100mmHg?

A

Pulmonary oedema:

Oxygen/CPAP
Furosemide
Vasodilator (nitrates etc)

± Inotrope if systolic BP is below 100mmHg

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19
Q

Rx for chronic heart failure- with left ventricular systolic dysfunction?

A

FAB DA

1st: Furosemide, ACEi, b-blocker
2nd: Digoxin, Aldosterone antagonist

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20
Q

Which b-blockers are licensed for heart failure?

Which one isn’t?

A

Bisoprolol
Carvedilol
Nebivolol

NOT Atenolol

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21
Q

A 70 year old gentleman who has had a previous MI gets a clinic BP reading of 145/91.
How should his BP be managed?

A

Calcium channel blocker (ie amlodipine, as over 55)

Give antihypertensive to anyone with Stage 1 HTN (>140/90) with: 
CVS disease
Diabetes
Renal disease
Organ damage who is under 80
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22
Q

Which patients should be offered a calcium channel blocker as 1st line treatment for their hypertension?

A

Those over 55 or black patients

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23
Q

What are the different stages of hypertension?

A

Stage 1: 140/90mmHg in clinic
Stage 2: 160/100mmHg
Stage 3: 180mmHg systolic
110mmHg diastolic

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24
Q 
What are the different BP targets for those 
Under 80
over 80
diabetic 
diabetic + end organ damage
diabetic + renal disease
A

Under 80 160/100 or CVS issue etc)

Over 80

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25
Q

Patient is on Amlodipine, Atenolol + Indapamide

It is noticed that their Potaassium is 4.2mmol/L

What should be done?

A

For HTN: B-blocker + CCB + thiazide + low K+

Spironolactone + expert advice

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26
Q

What defines postural hypotension?

A

A drop by 20mmHg in BP on standing compared to sitting/lying

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27
Q

How does heart failure lead to pitting oedema?

A

Reduced perfusion of the kidneys leads to salt and water retention and activation of the renin-angiotensin system, which increases water retention further

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28
Q

What pressure in the pulmonary system is indicative of pulmonary hypertension?

A

15-20mmHg

At 21-30mmHg interstitial oedema occurs

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29
Q

What’s the difference between defibrillation and cardioversion?

A

Defibrillation is non-synchronised shock (as ventricular fibrillation is not a regular pattern)

Cardioversion is synchronised shock, an unsynchronised one could lead to ventricular fibrillation (for AF, flutter, junctional tachycardia…)

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30
Q

Which cardiac abnormality requires dual pacing?

A

AV block

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31
Q

How long a PR interval is considered prolonged?

A

> 0.20 seconds (or 200ms)

5 little squares

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32
Q

What is the difference between Mobitz I and II and which is riskier?

A

Mobitz I- PR increases until dropped beat
Mobitz II- every 2/3rd beat is dropped, PR interval is constant

Mobitz II is more likely to progress to Mobitz III

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33
Q

ECG shows LBBB and left axis deviation. Which bundle (anterior or posterior) is affected?

A

Knock out of anterior bundle causes L ventricle to be depolarised from inferior to superior causing a Left Axis deviation

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34
Q

Patient has ECG with a HR of 130bpm and narrow QRS complexes. They are stable but having palpitations.

Management?

A

Supraventricular tachycardia

Valsalva manoeuvre, Carotid sinus massage…

2nd: IV adenosine

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35
Q

Why are vasodilators not as good in heart failure from diastolic dysfunction?

A

In diastolic dysfunction, the heart does not fill well in diastole as the heart may not relax in a normal manner.
High pressures are needed therefore to fill the heart, vasodilators lower pressure.

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36
Q

Symptomatic Rx of angina?

NB: not preventative

A

Glyceryl Trinitrate SL

B-blocker- slows heart
Ca channel antagonist- relaxes coronary arteries
Long acting nitrate isosorbide dinitrate

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37
Q

What occurs in acute coronary syndromes to cause the pain?

A

Rupture of a fibrous cap on the atheromatous plaque causes thrombus/emboli.

Platelets release Seratonin and thromboxane causing localised vasoconstriction, worsening ischaemia

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38
Q

What test can be done for those who come into hospital with MI-symptoms but on balance of Tropinin and ECG, FHx, PMH etc are deemed low risk, to determine prognosis?

A

Exercise test:

If negative = good prognosis

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39
Q

How do the different anti-platelet drugs work?

A

Aspirin- prevents thromboxane A2 formation needed to aggregation of platelets

Clopidogrel inhibits ADP activation of platelets

Abciximab + Eptifibatide - glycoprotein IIb/IIIa inhibitor (found on platelet surface)

Tirofiban- reversible glycoprotein IIb/IIIa inhibitor

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40
Q

How does Rivaroxiban and LMWH and unfractionated heparin work?

A

Novel anticoags- Rivaroxiban inhibits Xa directly

LMWH activates antithrombin- targets Xa

Unfractionated heparin- activates antithrombin- targets Xa and thrombin

X > Xa enables Prothrombin > Thrombin

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41
Q

What are the contraindications to b-blockers?

A

Asthma
AV block (as self-generating rhythm will be slowed further)
Acute pulmonary oedema

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42
Q

If fibrinolytic is given, how do you know whether it has failed to reperfuse and now needs re-thrombolysis or coronary angioplasty?

A

Less than 50% decrease in ST elevation after 90 minutes

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43
Q

Rx for ventricular tachycardia?

A

Amiodarone 300mg IV over 20 mins

Amiodarone 900mg over 24 hours

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44
Q

Long term management post MI?

AABC’S

A 
Aspirin
ACEi
B-blocker
Clopidogrel
Statin
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45
Q

What causes most mitral stenosis?

A

Rheumatic heart disease

Valves thicken, cusps fuse, calcium is deposited

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46
Q

Cause of a raised JVP with a normal waveform?

A

Fluid overload
Right heart failure

-unable to eject the venous return

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47
Q

Cause of raised JVP with absent pulse?

A

Superior vena cava obstruction

Backlog of blood from obstruction but is unrelated to heart contractions (not due to HF)

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48
Q

JVP has a large A wave, cause?

A

Pulmonary hypertension
Pulmonary stenosis

A wave is backflow of blood during atrial systole.
If ventricles are fuller, less blood goes from atria to ventricles, more backflow.

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49
Q

JVP with a cannon A wave

A

More severe than a large A wave:
Heart block

Atria contracts against a closed tricuspid valve

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50
Q

Cause of a JVP with an absent A wave?

A

Atrial fibrillation

No synchronised atrial systole

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51
Q

JVP with a large V wave?

A

Tricuspid regurgitation

V wave is ventricular systole, so atrial filling against a closed tricuspid valve. If tricuspid valve is leaky it allows more backflow as the atria fills from two directions.

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52
Q

Systolic murmurs louder on inspiration?

A

Tricuspid regurgitation
Pulmonary stenosis

L side during systolic

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53
Q

Freidrich’s ataxia is associated with which type of cardiac defect?

A

Hypertrophic (obstructive) cardiomyopathy

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54
Q

What signs are associated with HOCM?

A

S4 sound- as atria contracts against a stiff L ventricle
Jerky pulse
Double impulse at apex beat, as atria contracts and ventricle contracts as so hypertrophed

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55
Q

What kind of inheritance is hypertrophic cardiomyopathy associated with?

A

Autosomal dominant

Sarcomeric heavy chain or troponin gene mutation

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56
Q

Papillary muscle failure in the heart leads to prolapse of which valve?

A

Mitral valve

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57
Q

Of the systolic murmurs louder on expiration, which is louder with the valsalva manoeuvre and which is quieter?

A

L-sided systolic murmur (RILE)

Aortic stenosis is quieter- Valsalva increases pressure to expel blood out ventricle so less blood going past aortic valve

Mitral regurg is louder- more resistance to aortic outflow so more blood goes into atria

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58
Q

Which systolic murmur radiates to carotids?

A

Aortic stenosis (ejection systolic)

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59
Q

What signs of aortic stenosis indicate severity?

A

Presence of:
Slow rising pulse (limited flow)
Soft S2 sound (calcified valves are unable to slam shut)

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60
Q

What type of apex beat and pulse types are associated with aortic stenosis?

A

Heaving apex beat (due to hypertrophy)
Pulsus alternans- not all the blood gets evacuated
Slow-rising pulse- limited outflow

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61
Q

What heart sounds can be indicative of aortic stenosis?

A

Soft S2- calcified valves unable to slam shut
S4- hypertrophic ventricles vibrate as atria contracts
Split S2- slow outflow of L ventricle means P2 before A2

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62
Q

What is the difference cause of a thrUsting or Heaving apex beat?

A

Heaving in Hypertrophy- aortic stenosis, systemic hypertension

ThrUsting in flUid overload- aortic incompetence, mitral incompetence

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63
Q

Which treatments for heart failure help with symptoms but not mortality?

A

Furosemide and Digoxin

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64
Q

Patient has chronic heart failure, they are taking Ramipril, Carvedilol, Spironolactone and Digoxin, Furosemide PO and still they have breathlessness and swollen ankles.
What other options are there?

A

Salt and fluid restrict
bumetanide 1mg instead of furosemide (loop diuretic)
+ metolazone (thiazide)
IV furosemide

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65
Q

What treatments improve prognosis in angina?

And which one if someone has had a previous MI?

A

Aspirin
Simvastatin

Previous MI: b-blocker/CCB

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66
Q

Which treatments for angina improve symptoms but not prognosis?

A

GTN SL

If no previous MI:
B-blocker + CCB
if previous MI helps prognosis + symptoms

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67
Q

What are the different treatment approaches for permanent Af (lasting longer than 48 hours)

A

Rate control: b-blocker/ calcium channel blocker

Anticoagulate: Warfarin

Rhythm control: flecainide (normal heart), amiodarone (structural heart disease)

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68
Q

What ‘pill in the pocket’ is useful for paroxysmal AF?

A

Sotolol
Or
Flecainide

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69
Q

Someone has had palpitatios for the last four hours, and ECG shows AF, what anticoagulation would you use and why?

A

LMWH Dalteparin 5000 units

Warfarin will take too long to get up to a therapeutic dose whilst the patient is in acute AF (under 48 hours)

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70
Q

Want to cardiovert someone with acute AF, they have ischaemic heart disease. What drug should be used for medical cardioversion?

A

Amiodarone

If no IHD/WPW syndrome/normal heart
Flecainide

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71
Q

What are the stages of Fontaine’s peripheral arterial disease?

A

Stage 1: asymptomatic
Stage 2: intermittent claudication
Stage 3: ischaemic rest pain
Stage 4: ulceration/gangrene

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72
Q

CHAaDSsVasS Score?

A 
Cardiac failure
Hypertension >140/90
Age- 65 (1 point)
          75 (2 points)
Stroke (2 points)
          TIA (1 point)
Vascular disease- PAD, MI, aortic plauque
Sex- female (1 point)
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73
Q

Name for when JVP rises on inspiration (not normal)

And condition that causes it?

A

Kussmaul’s sign:
Inspiration reduces intrathoracic pressure increasing flow to the right side of the heart, unable to fit all the blood in restricted heart (due to constrictive pericarditis) so blood backlogs

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74
Q

Cause of a bounding pulse?

A

CO2 retention, liver failure and sepsis

Conditions causing low peripheral vascular resistance
(CO2 ret- autoregulation, liver failure- splanchnic circulation dilates)
Lead to low diastolic pressure and compensatory increased stroke volume so pulse is forceful and wide pulse pressure

75
Q

Causes of a collapsing pulse?

A

Aortic regurgitation
AV malformation
Patent ductus arteriosus

Ventricle is more full than normal = strong upshoot
Rapidly falling away as blood whooshes back in via defective valve

76
Q

Cause of bisferiens pulse?

A

Aortic stenosis with regurgitation:
Little blood coming out via ventricle, backflow of blood regurgitating back through valve allows for a second outflow pulse during systole.

77
Q

Difference between bisferiens pulse and pulsus alternans?

A

Bisferiens pulse is two pulses of blood outflow during systole, pulsus alternans = one strong then weak heart beat

Bisferiens: aortic stenosis + aortic regurgitation
Alternans: aortic stenosis, LV failure, cardiomyopathy

78
Q

What is the physiology behind pulsus paradoxus- systolic BP drops by 10mmHg on inspiration?

A

Inspiration- lowers thoracic pressure= increased blood flow to the R side of the heart + pulmonary vasculature expands leading to pooling of blood in the lungs and less L-sided output.
= reduced systolic BP

In cardiac tamponade, the R ventricle pressure may lead to septum being pushed into L ventricle reducing outflow,

79
Q

82 year old with chest pain and feeling unwell. Pale and nauseous.

What are the crucial tests to exclude serious things?

A

BP- asymmetric pulses in aortic dissection

ECG- ACS

Troponin- ACS

CXR: Widened mediastinum in aortic dissection
Clear in PE
Gas in the mediastinum for oesophageal tear

80
Q

How does management of AF differ if it has onset in the last 48 hours or longer ago than that?

A

In last 48 hours = acute
Give IV heparin and cardiovert (DC or pharmacologically)

Starting more than 48 hours ago
Anticoagulate for 4 weeks then DC cardiovert

81
Q

What features make cardioversion of AF more likely (rather than rate control)?

(Demographics, AF, HPC)

A

Under 65

Symptomatic
First presentation of lone AF

Haemodynamically compromised
Congestive cardiac failure

82
Q

What features make you more likely to rate control AF rather than try to cardiovert?

A

Over 65

Coronary artery disease
No congestive cardiac failure

83
Q

What are the causes of cardiomegaly?

Where the cardiac:thoracic ratio is greater than 50%

A

D: Neonates, infants and athletes
PC: cardiac dilation (HF etc), pericardial effusion
PMH: Skeletal abnormalities

84
Q

On an CXR how would cardiac effusion and heart failure look different?

A

Both would have cardiomegaly but in cardiac effusion the heart looks globular and there would not be associated change in vasculature, unlike heart failure

85
Q

Which part of the aorta becomes calcified in syphilitic aortitis compared to atherosclerosis?

A

Syphilis- ascending aorta

Atherosclerosis- descending aorta

86
Q

What causes pulmonary hypertension?

A

Lung: PE or chronic lung disease
Heart: mitral valve stenosis, LV failure, septal shunt from left to right

87
Q

Test for vagovagal syncope?

What counts as a positive result?

A

Upright tilt table test- bradycardia or hypotension following tilting and isoprenaline/GTN infusion

88
Q

What is the treatment for those with recurrent attacks of vagovagal syncope with proven reflex syncope?

A

Pacing (Not b-blockers)

Physical counter-pressure maneuvers - squatting, arm-tensing, leg crossing, when feel faint coming on

89
Q

When might an apex beat be non-palpable?

A

Obesity
Hyper-expanded chest (COPD)
Dextrocardia

90
Q

If someone is haemodynamically unstable and the heart rate is very slow, what drug can be given to speed it up?

A

Atropine (anticholinergic to counter parasympathetics)

0.5mg every 3-5 mins

91
Q

What is a prolapsing mitral valve associated with?

Hear an ejection click and mitral regurgitation

A

Marfan’s and other connective tissue disorders (Ehlers-Danlos)
Thyrotoxicosis
Rheumatic fever (group A strep), endocarditis

92
Q

A gentleman comes in, you notice he has long arms and long spidery fingers and a pectus deformity.
What is he at danger of and what are other features of this condition?

A

Marfan’s- poor elastic fibres

Aortic dissection/dilatation- can use b-blockers to slow dilatation
Mitral valve prolapse

Head: Lens dislocation, high-arched palate,
Shoulders: Scoliosis, Dural ectasia (ballooning of dural sac around spinal cord)
Knees: joint hypermobility
Toes: pes planus

93
Q

Gentleman with Marfan’s syndrome has been identified as having growing aortic dilatation. What medication can be offered to slow progress?

A

beta-blockers

94
Q

What organisms commonly cause infectious endocarditis in people with native valves?

A

Staph aureus
Strep viridans (not S. Pneumo)
Enterococcus

95
Q

Which risk factor is particularly associated with R-sided valve endocarditis in native valves?

A

IV-drug users as venous access seeds to the valve.

96
Q

What is the pathogenesis for the sequalae of infective endocarditis (splinter haemorrhages, Roth spots etc)?

A

Where immune complexes (Ig + antigen) get deposited, it causes vasculitis and small haemorrhages:
Osler’s nodes (ow- fingers), Janeway lesions (“WAY?!” High five- on palms, flat from high 5ing)

97
Q

A gentleman has a fever and a recent onset heart murmur that has not been noted before. What needs to be considered and how can it be investigated?

A

Infective endocarditis

Blood cultures, echo (look for vegetations)
ECG: emboli can cause MI, conduction defects may arise

98
Q

2 major criteria that have to be fulfilled to diagnose definite infective endocarditis can be:

A

Positive blood culture
Typical organism in 2 separate cultures
Persistently +ve blood cultures, ie 3/3, 12 hours apart

Endocardium involved
Positive echo- vegetation, abscess
New valvular regurgitation- not just a change in murmur

99
Q

3 minor criteria + 1 major criteria (blood cultures, echo, valve regurgitation) enable a diagnosis of infective endocarditis according to Duke’s criteria. What are the minor criteria?

A

Predisposition- heart condition, IV drug use

PC: Fever >38 degrees
Vascular sequelae- septic PE, janeway lesions, mycotic aneurysm
Immunologic sequalae- Osler’s node, Roth spots, glomerulonephritis

IHx: +ve blood culture (not major enough)
+ve echo (not major enough)

100
Q

Rx for native valve infectious endocarditis (organism unknown)

A

Amoxicillin ± Gentamycin

101
Q

Rx for prosthetic valve infectious endocarditis where organism is not known

A

Vancomycin + Gentamycin + Rifampicin

102
Q

Suspect a pulmonary embolism? Gold standard investigation?

Who can’t have this?

A

CT-PA

CT pulmonary angiogram
Uses contrast so not appropriate for impaired kidney function patients

103
Q

You identify a massive PE on CT-PA. The patient says the breathlessness onset 2 hours ago.

BP: 90/50
How can it be managed?

A

Massive PE + evidence of acute heart strain (low BP):

Thrombolysis: Streptokinase/Alteplase

If less acute/urgent- anticoagulation: LMWH instead

104
Q

Which score determines the likelihood of a PE?

A

Well’s score

Above 6 = high likelihood

105
Q

What causes myocarditis?

A

Commonly viral- Coxsackie virus

Diptheria
Rheumatic fever- Strep A
Radiation injury

106
Q

Patient has fever and biventricular failure (oedema of ankles and pulmonary oedema)

ECG shows nonspecific ST changes
CXR- cardiac enlargement

What could be going on?

A

Myocarditis
Only viral

Management: bed rest + treat heart failure

107
Q

What would you find on an echo that would suggest a patient is getting heart failure because of dilated cardiomyopathy rather than it being due to ischaemia?

A

Dilated cardiomyopathy- global hypokinesis

Ischaemia- focal/regional impaired contraction

108
Q

What are the stages of the New York functional classification of heart failure?

A

I- No limitation of physical activity, no fatigue, SOB, palpitation

II Comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea.

III Less than ordinary activity causes fatigue, palpitation, or dyspnea.

IV Unable to carry on any physical activity without discomfort. Symptoms of heart failure at rest.

109
Q

When going up stairs a patient complains of shortness of breath and palpitations. What stage of New York Functional classification of heart failure is this?

A

Stage II:

I No limitation of physical activity, no fatigue, SOB, palpitation

II Comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea.

III Less than ordinary activity causes fatigue, palpitation, or dyspnea.

IV Unable to carry on any physical activity without discomfort. Symptoms of heart failure at rest.

110
Q

Leading cause of dilated cardiomyopathy in South America?

Clue: infectious
What anatomical defect is pathognomonic?

A

Chagas disease:
Trypansoma cruzi- a protozoa

Left ventricular apical aneurysm
(Get acute myocarditis, cardiac enlargement, tachycardia etc)

111
Q

What anatomical/functional features define dilated cardiomyopathy?

A

Left ventricular chamber enlargement
Systolic dysfunction (heart failure)
Normal left ventricular wall thickness

Echo: global hypocontractility

112
Q

Typically what is the difference in cardiac dysfunction observed in dilated cardiomyopathy compared to hypertrophic cardiomyopathy?

A

In dilated CM the lack of contractility leads to systolic failure.
In hypertrophic CM the enlarged interventricular septum leads to impaired filling and therefore a diastolic dysfunction

113
Q

What is the pathophysiology of hypertrophic cardiomyopathy?

What happens anatomically?

A

Gene mutations in sarcomeric proteins (actin, myosin heavy chain etc)

Abnormal myofibril arrangement and fibrosis of the heart tissue, leading to hypertrophy (diastolic dysfunction, LV outflow obstruction, mitral regurgitation)

Often with narrowed coronary arteries due to thickening of the intima (may cause ischaemia)

114
Q

Inheritance pattern of familial hypertrophic cardiomyopathy?

A

Autosomal dominant

HYPERTROPH IS DOMINANT

115
Q

What can be the cause of a different blood pressure in each arm?

A

coarctation of aorta, subclavian steal aortic dissection
peripheral vascular disease
unilateral neuromuscular abnormalities

116
Q

What gene, if mutated will cause familial aortic stenosis?

A

Elastin gene

117
Q

In exercise ECG testing what comprises a positive result?

A

A horizontal or down-sloping ST depression.

An upsloping ST depression doesn’t count

118
Q

A patient is undergoing a diagnostic cardiac catheterisation when an assistant notices the loss of the peripheral pulse, what could be the cause?

A

Dissection, thrombosis or arterial spasm

119
Q

Mechanism of Aspirin?

A

Irreversibly inhibits cyclo-oxygenase enzymes in platelets, preventing thromboxane A2 production and platelet aggregation.
(TxA2 triggers expression of GpIIb/IIIa needed for platelet conformation changes for aggregation)

120
Q

What are the different roles of B1 and B2 adrenergic receptors?

A

B1 = inotropic + chronotropic (bisoprolol is selective)

B2 = peripheral vasocontriction + bronchoconstriction

121
Q

Which different transporters do loop, thiazide and potassium sparing diuretics act on?

A

Loop = Na/2Cl/K co-transporter
Thiazide = Na/Cl co-transporter
K+ sparing = ENaC distally, H/Na exchanger proximally

122
Q

Metabolic SEs of different types of diuretic?

A

Loop- low K, low Ca
Thiazide- low K, high Ca, low Mg, high urate

K is low because more Na in the cortical collecting duct allows for exchange via ENaC

123
Q

What are the two different types of Ca channel blockers and which drug is CI with one type?

A

Dihydropyridines: nifedipine, amlodipine =peripheral vasodilators

Non- dihydropyridines: verapamil, diltiazem =slow AV + SA node conduction

Don’t give verapamil with b-blockers (profound bradycardia/HF)

124
Q

What’s the mechanism of Digoxin?

A

Na/K/ATPase pump takes K in and Na out.
Na/Ca exchanger takes Na in and Ca out.

Without lots of Na outside, can’t swap it for Ca so more Ca in heart muscle, stronger contraction

125
Q

How do statins work?

A

Inhibit HMG-CoA reductase which recycles cholesterol so it all has to be made from scratch in the liver.
The lower levels of cholesterol trigger more LDL receptor expression in hepatocytes increasing LDL uptake and reducing blood levels

126
Q

What kind of ACEi is best suited to the elderly?

A

Long acting ones like Lisinopril

1st dose can cause hypotension, best taken at night

127
Q

What kind of change in BP as an ACE inhibitor is starter would make you worry about renal artery stenosis?

A

> 20% rise in creatinine

>15% decrease in GFR

128
Q

How is the management different for those with Prinzmetal angina compared to normal angina?

Printzmetal angina is caused by coronary artery spasm rather than coronary artery disease

A

Rx: CCB ± long acting nitrates

Avoid aspirin (aggravates ischaemia) 
And b-blockers (increase vasospasm)
129
Q

What conditions are included in acute coronary syndrome?

A

Unstable angina and evolving MI
Both due to plaque rupture, thrombosis and inflammation

Can also be due to emboli/coronary spasm of normal arteries or vasculitis

130
Q

How do silent MI’s present in the elderly or diabetic?

A 
Nausea, sweatiness, palpitations
Dyspnoea
Syncope, acute confusion
Pulmonary oedema
Epigastric pain/vomiting etc
131
Q

Why does creatinine kinase-MM become raised?

A 
From skeletal muscle
Falls, seizures, prolonged exercise
Myositis
Hypothyroidism
Afro-caribbean
132
Q

Suspect MI from history, immediate management?

Rx not IHx

A

Morphine (+ metoclopramide)
O2
Nitrates
Aspirin 300mg to chew

133
Q

For patients that have acute coronary syndrome without ST elevation, but are high risk (recurrent iscahemia, ST depression, diabetes, high troponin) what medication should you give them, and within how many hours should they receive angiography?

A

A GPIIb/IIIa antagonist and angiography within 96 hours (4 hours)

134
Q

If someone develops 1st degree AV block following an inferior MI what medication may need to be stopped if things deteriorate further?

A

If second degree heart block develops, CCB and b-blockers will need to be stopped

135
Q

Patient has an MI and then develops sustained VT for 2 minutes, how should they be managed?

A

If compromised DC cardiovert, if stable amiodarone

Amiodarone reduces Ca inflow to prolong repolarisation and slow the heart. It acts like a b-blocker on SAnode further slowing pace.

136
Q

Rx for pericarditis following an MI?

A

NSAIDs

137
Q

A patient takes amiodarone daily for his ventricular tachycardia, what monitoring IHx does he need to check up on the common side effects?

A

LFTs- hepatits
TFT- raises T4, lowers T3
Corneal deposits, photosensitivity
Lung fibrosis

138
Q

How is Rx different for acute and chronic heart failure?

A

Acute: SYMPTOMATIC
Furosemide, morphine, GTN

Chronic: B-blocker, ACEi
(Then spironolactone or ARB. Then digoxin or cardiac resynchrony)

139
Q

What is the Rx hierarchy for hypertension

A

ACEi (young + white) or CCB/thiazide (>55 or black)

A+C or D
A+C+D
A+C+D +b-blocker/a-blocker/diuretic

140
Q

Rx for someone who has had palpitations for the last 30 hours, BP 80mmHg found to have AF, never had it before?

A

Unstable acute AF
Cardiovert: Flecainide (normal heart)
Amiodarone (IHD or structural abnormality)

Rate control: b-blocker or CCB

LMWH

141
Q

What Rx should be offered for CHAADSSVasS scores (calculated for those with AF)?

A

Score 0 = no therapy

Score 1 = warfarin or NOACs

142
Q

What does HASBLED stand for?

A 
Hypertension (>160/uncontrolled)
Abnormal renal (1) or liver (1) function
Age >65
Stroke
Bleeding disorder
Labile INR
Extra drugs- antiplatelets/NSAIDs
Drugs/alcohol use

Score>3 warrants more regular review

143
Q

Which part of the heart do Digoxin, b-blockers and ca channel blockers exert their effects on to slow the heartbeat?

A

Reduce AV nodal conduction

144
Q

In those with AF who have wolff parkison white, which standard Rx can you not give?

A

Flecainide to cardiovert

B-blockers/CCBs to rate control as causes bradycardia

145
Q

Supraventricular tachycardia is not responding to adenosine, what is next line Rx?

A

Beta blocker or Ca channel blocker (not both)

146
Q

What is the different uses and mechanism of adenosine, atropine and amiodarone?

A

Adenosine terminates AV node re-entrant tachycardias (binds to AV node to transiently block it)

Atropine is used in bradycardias (anticholinergic to block vagal input)

Amiodarone prolongs action potential (reduces calcium permeability, slows AVnode conduction) used to cardiovert

147
Q

What metabolic abnormalities can cause ventricular tachycardia?

A

Low K+, low Mg2+

148
Q

What heart rhythms are shockable or non-shockable during ALS?

A

Shockable: ventricular fibrillation, pulseless VT

Non-shockable: pulseless electrical activity, asystole

149
Q

During ALS what drug should you give and how often?

A

Adrenaline every 3-5 minutes

150
Q

What are the reversible causes of cardiac arrest?

4 H’s, 4 T’s

A

Hypothermia
Hypovolaemia
Hypoxia
Hypo/Hyperkalaemia

Tamponade
Tension pneumothorax
Thrombosis
Toxins

151
Q

What are the indications for a CABG that prolong survival?

A

Triple vessel disease

Left main stem (L coronary artery) disease

152
Q

Patient keeps getting episodes of SVT and then bradycardia. What is the cause and potential management?

A

Tachy-brady syndrome occurs in sick sinus syndrome (sinus node dysfunction)

Requires pacing if symptomatic

153
Q

How does sinus tachycardia and SVT look different on ECG?

A

Sinus tachy- p waves normal

SVT- p waves absent or inverted (due to the pace being set from the AVN and conducting through the atria retrograde)

154
Q

Morphology of P waves looks different (at least 3 distinct appearances) and P-P intervals are irregular. HR is 140.

What is the name of this and what disease is it associated with?

A

Multifocial atrial tachycardia

COPD- Rx hypoxia and hypercapnia

155
Q

What findings on an ECG suggest a broad complex tachycardia may be ventricular tachycardia?

A

Positive QRS concordance in chest leads (all up/all down)
Left axis deviation
AV dissociation
Fusion beat (normal beat fuses with VT complex)
Capture beat (normal beat between VT complexes)

156
Q

Rx for torsades de pointes (polymorphic VT)

A

Magnesium sulphate over 5mins

+ DV cardiovert

157
Q

What are the indications for a permenant pacemaker?

A 
Type 3 or Mobitz type 2 AV block (regularly missing beats)
Symptomatic bradycardias
Heart failure (can have biventricular to resynchronise)
Drug-resistant tachyarrhythmias (can have a defibrillator in it)
158
Q

What causes diastolic heart failure?

A

If the ventricles can’t relax sufficiently to allow filling:
Ejection fraction may be normal

Constrictive pericarditis, tamponade
Restrictive cardiomyopathy
Hypertension

159
Q

What investigations are suggestive or definitive of heart failure?

A

Suggestive: ECG abnormality, BNP (actually most accurate)
Definitive: echocardiography

160
Q

CXR signs of heart failure?

A 
Alveolar oedema (bat wing shadowing)
Kerley B lines (interstitial oedema)
Cardiomegaly
Dilated upper lobe vessels
Pleural Effusion
161
Q

How does the presence of symptoms stratify heart failure severity In the New York Heart Association grading?

A

1- no symptoms on ordinary activity
2- symptoms of ordinary activity
3- symptoms with less than ordinary activity
4- symptoms at rest

162
Q

Causes of secondary hypertension?

A

Renal interstitial: glomerulonephritis, PAN, systemic sclerosis, polycystic kidneys, chronic pyelonephritis

Renal vascular: atheroma, fibromuscular dysplasia

Endo: Conn’s (aldoesterone), Cushing’s (cortisol), phaeochromocytoma (adrenaline), acromegaly (GH), high PTH

Drugs: steroids, the pill
Coarctation, pregnancy

163
Q

Tests for secondary causes of hypertension?

A

U+E: low K (Conn’s) or high Ca (PTH)
BM: acromegaly
Urine dip: glomerulonephritis

Renal USS: renal a stenosis
MR: coarctation aorta
Urinary metanephrines (phaeo), free cortisol (Cushings)
Renin, aldoesterone (Conn’s)

164
Q

Which cardiovascular drugs increase the risk of gout?

A

Thiazide diuretics

165
Q

Jones criteria of rheumatic fever:

(Recent strep infection and:
2 major
Or 1 major and 2 minor)

A

Group A b-haemolytic Strep infection:
+ve throat culture, strep antigen test +ve, rising strep antibody titre, recent scarlet fever

Major: (CASES)
Carditis, arthritis, subcutaneous nodules, erythema marginatum (truncal red raised rash), syndenhams chorea

Minor:
Fever, raised ESR, arthralgia, long PR, PMH rheumatic fever

166
Q

Features of salicylate toxicity (ie aspirin)

A

Tinnitis
Metabolic acidosis
Hyperventilation

167
Q

Which valve is most commonly affected in rheumatic heart disease?

A

Mitral

168
Q

Signs of mitral stenosis

A

Diastolic murmur
Loud S1 (atria still getting blood out when valve shuts)
Tapping apex beat (L atria large and moves LV closer to hand to make apex beat more palpable)

169
Q

What is a graham steell murmur?

A

Pulmonary regurgitation secondary to pulmonary hypertension secondary to mitral stenosis

170
Q

What are the heart sounds of mitral regurgitation and why?

A

Pansystolic murmur radiating to axilla
Soft S1, mitral leaflets don’t meet
Split S2, LV emptying happens quicker as blood can exit from aorta and atria
Loud S3, atria overfilled, rapid ventricular filling

ThrUsting apex beat- mitral regUrgitation

171
Q

How does aortic stenosis present?

A

Angina
Syncope
Exertional dyspnoea/HF

Dizziness/faints…

172
Q

What are the eponymous signs of aortic regurgitation?

A

Corrigan’s- carotid pulsation
De Musset’s- head nodding with heart beat
Quincke’s- capillary pulsations in nail bed
Traube’s- pistol shot sound over femoral artery
Austin Flint murmur (low rumbling mid diastolic murmur=severe, the normal AR murmur is early diastolic, high pitched)

173
Q

Intrinsic and extrinsic causes of acne?

A

Intrinsic
Hormonal: PCOS, virilising tumours, congenital adrenal hyperplasia, Cushing’s, acromegaly

Medical: steroids (increase keratinisation of ducts), combined pill (raise testosterone), phenytoin, lithium
Isoniazid, ciclosporin

Extrinsic: oils, coal, tar, weed killer

174
Q

Name of the bacteria in acne?

A

Propionibacterium acnes

175
Q

Pregnant woman with moderate acne, what can be given, what should be avoided?

A

CI: Tetracycline antibiotic
Erythromycin, trimethoprim = fine

CI: Oral retinoids, isotretinoin

176
Q

Rx of mild comedonal acne?

A

Topical retinoids (adapalene, tretinoin, isotretinoin)
Salicylic acid
Azelaic acid

177
Q

Rx of mild inflammatory (papulo-pustular) acne?

A 
Topical retinoid (adapalene, tretinoin, isotretinoin)
Topical Abx (doxycycline, tetracycline, minocycline)
Benzoyl peroxide
178
Q

Rx of moderate inflammatory (papulo-pustular acne)

A 
Topical retinoid (adapalene, tretinoin, isotretinoin)
Oral antibiotics (tetracycline, minocycline)
179
Q

Rx of severe nodulocystic acne (cysts, abscesses, scarring)

A

Oral retinoid (isotretinoin)

Or contraceptive co-cyprindiol pill (high oestrogen, low testosterone)

180
Q

Why does ST depression on an ECG stress test suggest coronary artery disease?

A

Ischaemia not affecting the whole wall, the injured cells are closer to the inner part of the heart (sub-endocardium). They do not depolarise as much as healthy cells, so the current flows from +ve charged depolarised cells to the inner part of the heart, during ST segment.
Anterior chest leads detect current flowing away from them (therefore ST depression)

181
Q

RV cardiomyopathy + curly wool hair + palmoplantar keratosis on feet, is known as which disease?

A

Naxos disease- inherited in those of Mediterranean descent, autosomal recessive
PC: SOB, blackouts, poor exercise tolerance

182
Q

Type of cardiomyopathy that may follow pre-eclampsia?

A

Dilated cardiomyopathy

183
Q

Autoimmune associated cardiac disease where biopsy shows bands of necrosis surrounded by inflammatory infiltrate?

A

Giant cell myocarditis- rare

184
Q

How does the site of a dissecting aorta determine your management approach?

A

Type A (2/3rds) in the ascending aorta require surgical management with blood pressure control (due to potential to affect carotid perfusion)

Type B (1/3rd) in the descending aorta may be conservatively managed with bed rest and reducing blood pressure with IV labetalol

Fifth Year Medicine (32 decks)

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