Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 3: Medicine Block CARDIORESPIRATORY year 5 > General Cardiology > Flashcards

General Cardiology Flashcards

1
Q

What is the mechanism of action of Statins?

A

Statins inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are adverse effects of Statins?

A
  • Myopathy
  • Liver impairment
  • Increased risk of Intracereberal haemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the myopathies caused by Statins?

A
  • Types
    • Myalgia
    • Myosistis
    • Rhabdomyolysis
    • Asymptomatic Raised Creatine Kinase
  • Myopathy is more common in lipophilic statins (simvastatin, atorvastatin) than relatively hydrophilic statins (rosuvastatin, pravastatin, fluvastatin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is liver impairment managed in statins?

A
  • Check LFTs at baseline, 3 months and 12 months.
  • Treatment should be discontinued if serum transaminase concentrations rise to and persist at 3 times the upper limit of the reference range
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Who should receive statins?

A
  • All people with established cardiovascular disease (stroke, TIA, ischaemic heart disease, peripheral arterial disease)
  • Following the 2014 update, NICE recommend anyone with a 10-year cardiovascular risk >= 10%
  • Patients with type 2 diabetes mellitus should now be assessed using QRISK2 like other patients are, to determine whether they should be started on statins
  • Patients with type 1 diabetes mellitus who were diagnosed more than 10 years ago OR are aged over 40 OR have established nephropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the statin used as Primary Prevention?

A

Atorvastatin 20mg OD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When should statins be taken?

A
  • Statins should be taken at night as this is when the majority of cholesterol synthesis takes place.
  • This is especially true for simvastatin which has a shorter half-life than other statins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How are statins used as Secondary Prevention?

A

Atorvastatin 80mg OD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are nitrates?

A
  • Nitrates are a group of drugs which have vasodilating effects
  • Work on Veins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the mechanism of action of Nitrates?

A
  • Causes release of nitric oxide in smooth muscle, increasing cGMP which leads to a fall in intracellular calcium levels in angina which both work to dilate the coronary arteries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are side effects of Nitrates?

A
  • Hypotension
  • Tachycardia
  • Headaches
  • Flushing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How should Nitrate tolerance be managed?

A

Patient develop tolerances and experience reduced efficacy

  • Patients who develop tolerance should take the second dose of isosorbide mononitrate after 8 hours, rather than after 12 hours.
  • Allows blood-nitrate levels to fall for 4 hours and maintains effectiveness
  • Effect is not seen in patients who take modified release isosorbide mononitrate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is adenosine used for?

A

Used to terminate supraventricular tachycardias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What can enhance and block effects of adenosine?

A
  • Adenosine are enhanced by Dipyridamole (antiplatelet agent)
  • Blocked by Theophyllines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When should adenosine be avoided?

A

Avoided in asthmatics due to possible bronchospasm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the mechanism of action of Adenosine?

A
  • Causes transient heart block in the AV node
  • Agonist of the A1 receptor in the atrioventricular node, which inhibits adenylyl cyclase thus reducing cAMP and causing hyperpolarization by increasing outward potassium flux
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the half life of adenosine?

A

8-10 seconds

  • Ideally be infused via a large-calibre cannula due to it’s short half-life,
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are some side effects of Adenosine?

A
  • Chest pain
  • Bronchospasm
  • Transient flushing can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is a Syncope?

A
  • Defined as a transient loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery.
20
Q

What are the types of Syncope?

A
  • Reflex syncope (neurally mediated)
  • Orthostatic syncope
  • Cardiac syncope
21
Q

What causes Reflex Syncope?

A
  • Vasovagal: triggered by emotion, pain or stress. Often referred to as ‘fainting’
  • Situational: cough, micturition, gastrointestinal
  • Carotid sinus syncope
    • Most common cause
22
Q

What causes Orthostatic Syncope?

A
  • Primary Autonomic Failure: Parkinson’s disease, Lewy body dementia
  • Secondary Autonomic Failure: e.g. Diabetic neuropathy, amyloidosis, uraemia
  • Drug-induced: diuretics, alcohol, vasodilators
  • Volume Depletion: haemorrhage, diarrhoea
23
Q

What causes Cardiac Syncope?

A
  • Arrhythmias:
    • ​Bradycardias (sinus node dysfunction, AV conduction disorders)
    • Tachycardias (supraventricular, ventricular)
  • Structural:
    • Valvular
    • Myocardial infarction
    • Hypertrophic obstructive cardiomyopathy
  • Others:
    • Pulmonary Embolism
24
Q

How do you assess syncope?

A
  • Cardiovascular examination
  • Postural blood pressure readings
    • Symptomatic fall in systolic BP > 20 mmHg or diastolic BP > 10 mmHg or decrease in systolic BP < 90 mmHg is considered diagnostic
    • ECG
    • Carotid sinus massage
  • Tilt table test
    • 24 hour ECG
25
Q

What is Pulsus Paradoxus?

A

Greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration

26
Q

What causes Pulsus Paradoxus?

A
  • Severe asthma
  • Cardiac tamponade
27
Q

What causes a Slow-rising pulse?

A

Aortic Stenosis

28
Q

What causes a collapsing pulse?

A
  • Aortic Regurgitation
  • Patent ductus arteriosus
  • Hyperkinetic States (anaemia, thyrotoxic, fever, exercise/pregnancy)
29
Q

What causes Pulsus Alterans?

A
  • Regular alternation of the force of the arterial pulse
  • Severe LVF
30
Q

What causes Bisferiens Pulse?

A
  • ‘double pulse’
  • Two systolic peaks
  • Mixed Aortic Valve Disease
31
Q

What are pulses for HOCM?

A
  • Jerky Pulse
  • Bisferiens pulse
32
Q

What causes Ejection systolic mumurs?

A
  • Aortic Stenosis
  • Pulmonary Stenosis
  • Hypertrophic obstructive cardiomyopathy atrial septal defect, tetralogy of Fallot
33
Q

What causes late systolic?

A
  • Mitral valve prolapse
  • Coarctation of aorta
34
Q

What causes early diastolic murmurs?

A
  • Aortic Regurgitation
    • high-pitched and ‘blowing’ in character
  • Graham-Steel murmur
    • pulmonary regurgitation, again high-pitched and ‘blowing’ in character
35
Q

What causes mid-late diastolic murmurs?

A
  • Mitral stenosis
    • ‘rumbling’ in character
  • Austin-Flint murmur
    • severe aortic regurgitation, again is ‘rumbling’ in character
36
Q

What causes continuous machine-like murmur?

A

Patent ductus arteriosus

37
Q

What gives an S1 heart sound?

A
  • Closure of mitral and tricuspid valves
    • Soft in Long PR or Mitral Regurgitation
    • Loud in mitral stenosis
38
Q

What gives an S2 heart sound?

A
  • Closure of Aortic and Pulmonary valves
    • Soft in aortic stenosis
    • Splitting during inspiration is normal
39
Q

What gives an S3 heart sound?

A
  • Caused by diastolic filling of the ventricle
    • Considered normal if < 30 years old (may persist in women up to 50 years old)
  • Heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock) and mitral regurgitation
40
Q

What gives an S4 heart sound?

A
  • May be heard in Aortic stenosis, HOCM, hypertension
    • Caused by atrial contraction against a stiff ventricle in HOCM a double apical impulse may be felt as a result of a palpable S4
41
Q

What are some abnormal waves on ECG?

A
  • Q waves are associated with a previous myocardial infarction
  • Delta waves are associated with Wolff-Parkinson-White Syndrome
  • Saddle ST elevation is associated with pericarditis
42
Q

What are normal variants on the ECG?

A
  • Sinus arrhythmia
  • Right axis deviation (tall and thin individuals)
  • Left axis deviation (short, obese individuals)
  • Partial right bundle branch block
43
Q

What are additional normal variants seems in athletes?

A
  • Sinus bradycardia
  • 1st degree atrioventricular block
  • Wenckebach phenomenon (2nd degree atrioventricular block Mobitz type 1)
  • Junctional escape rhythm
44
Q

What are risk factors for myopathy in Statins?

A

Risks factors for myopathy include:

  • Advanced age
  • Female sex
  • Low body mass index
  • Presence of multisystem disease such as diabetes mellitus.
45
Q

What are the effects of Nitrates on the heart?

A
  • Causes Venous Dilation
  • Reduces Venous return which in turn
  • Reduces left ventricular work so reduced preload
  • Reducing myocardial oxygen demand

Year 3: Medicine Block CARDIORESPIRATORY year 5 (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions