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Cardiovascular Flashcards

1
Q

What is primary prevention in the context of CVD?

A

The management of risk factors prior to the overt demonstration of CVD (assessing the patient’s risk and initiating management to prevent CVD)

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2
Q

What is secondary prevention in the context of CVD?

A

The management principles that must be applied after CVD has manifested (what needs to be done to minimise escalation of disease)

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3
Q

What is tertiary prevention in the context of CVD?

A

Management aimed at reducing the incidence of chronic incapacity or recurrence of disease, and the functional consequences of an illness (how to maximise patient wellbeing and prevent disease recurrence)

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4
Q

What does ‘absolute risk’ refer to in CVD risk management?

A

The numerical probability of a CVD event occuring within 5 years, expressed as a percentage (accounts for the combined effect of multiple risk factors)

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5
Q

True or false? With regards to CVD risk management, evidence shows that moderate reduction in several risk factors is more effective than a major reduction in one factor?

A

True

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6
Q

What is the target group for calculating absolute CVD risk in Australia?

A

All adults 45 years and above without known history of CVD, and ATSI peoples 35 and above

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7
Q

List at least 5 modifiable risk factors for CVD

A

Smoking, BP, lipids, waist circumference and BMI, nutrition, physical activity and alcohol intake

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8
Q

List at least 3 non-modifiable risk factors for CVD

A

Age, sex, family history of premature CVD, social factors including culture/ethnicity/SES and mental health

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9
Q

List at least 4 conditions that preclude individuals from CVD risk assessment using the Framingham criteria because they are already known to be at clinically determined high risk

A

Diabetes and >60 years
Diabetes with microalbuminuria (UAR >2.5 for men and >3.5 for women)
Moderate/severe CKD (persistent proteinuria or eGFR <45)
Previous diagnosis of familial hypercholesterolaemia
SBP >180, DBP >110
Total cholesterol >7.5
ATSI over age 74

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10
Q

For patients at High Risk of CVD as per the FRE, what are the targets for BP?

A

<140/90 in general or for CKD;

<130/80 for diabetics with micro or macro albuminuria (UACR >2.5 in men and >3.5 women)

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11
Q

What are the lipid targets for primary prevention of CVD?

A

TC <4; Triglycerides <2; HDL >1; LDL <2 (LDL <1.8 in diabetes and CAD)

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12
Q

What is the diet advice to reduce CVD risk?

A

Dietary Guidelines for all Australians - varied diet;
Limit saturated and transfats
Limit salt to <6g/day
Limit ETOH to <10 SD per week and no more than 4 on any one occasion

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13
Q

What is the physical activity advice to reduce CVD risk?

A

At least 30 mins moderate intensity exercise on most/all days of the week (or 150 mins/week) + 2-3 sessions (60 mins) resistance training per week

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14
Q

What is the weight advice to reduce CVD risk?

A

Limit energy intake to maintain healthy weight

Ideally BMI < 25 and waist circumference <94 in men and <80 in women

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15
Q

List the 2 anti-HTN drug combinations that should be avoided in treatment of hypertension

A
  1. Potassium sparing diuretics (spironolactone) plus ACE/ARB
  2. Beta blocker plus verapamil
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16
Q

In diabetic patients, if an ACE/ARB does not sufficiently reduce BP, which 2 antihypertensives should be considered as second line?

A

CCBs or thiazide

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17
Q

To treat hyperlipidaemia in a patient who is intolerant to statins, which 3 other drug may be considered?

A

Ezetimibe, bile acid binding resin or nicotinic acid

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18
Q

If triglyceride levels are not sufficiently reduced on maximally tolerated doses of statin, which 3 additional drugs may be added?

A

Fenofibrate (especially if HDL is below target), nicotinic acid or fish oil

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19
Q

In ATSI peoples without existing CVD, risk factor screening should commence at the age of ____ at the latest

A

18 (and the calculator from age 30)

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20
Q

List at least 3 indications for ambulatory BP monitoring

A
  1. Suspected white coat HTN
  2. Suspected nocturnal HTN or no night time dipping
  3. HT despite appropriate tx
  4. Hx risk of CVD even in clinic BP normal
  5. Suspected episodic HTN
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21
Q

Describe how to appropriately select the arm used for ambulatory BP measurements.

A

Measure BP in both arms. If less than 10mmHg SBP difference, use the non dominant arm, if greater than 10mmHg difference, measure in the arm with the higher pressure

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22
Q

Quote the ambulatory BP measurements for a 24 hour period that signify hypertension

A

24 hour average <130/80
Day time <135/85
Night time <120/75

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23
Q

Normal night time SBP and DBP should be in what range?

A

At least 10% below daytime average

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24
Q

What is BP load in regards to ambulatory BP monitoring? What is the normal limit?

A

Refers to the percentage of time that BP readings exceed HTN values during 24 hours, should be <20% of the time

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25
Q

True or false? The treatment targets based on ABP are lower than the targets for clinic BP readings?

A

True

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26
Q

Name a situation in which ambulatory BP may be inaccurate

A

In a patient with arrhythmia - it will not detect this.

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27
Q

People with ‘white coat hypertension’ are at increased risk of developing which 2 disorders?

A

Hypertension and glucose intolerance.

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28
Q

When should BP medication be started in a patient with low CVD risk?

A

If BP persistently above 160/100

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29
Q

When should BP medication be started in a patient with moderate CVD risk?

A

If BP persistently above 140/90

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30
Q

Once decided to treat, patients with uncomplicated hypertension should be treated to a target of what?

A

<140/90, or lower if tolerated

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31
Q

In selected high-risk patients, where BP is being targeted to <120 systolic, close follow-up is recommended to screen for which related adverse effects?

A

Hypotension, syncope, electrolyte abnormalities and AKI

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32
Q

In patients with uncomplicated HT, which drugs are suitable first-line options?

A

ACE, ARB, CCB, thiazides

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33
Q

For which class of anti-HT is the balance between efficacy and safety less favourable?

A

Beta blockers

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34
Q

What is the BP target for patients with HTN and a history of TIA or stroke?

A

<140/90

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35
Q

What drugs should be considered as first-line therapy for HTN in patients with CKD in the presence of albuminuria?

A

ACE or ARB

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36
Q

When should patients with CKD be commenced on an anti-hypertensive? What is the treatment target for these patients?

A

When BP consistently >140/90, and treated to target of less than this (although aiming towards <120 has shown benefit when tolerated)

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37
Q

For patients with a history of MI, which 2 drug classes are recommended for the treatment of HTN and secondary prevention?

A

ACE and beta blockers

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38
Q

Which 2 classes of anti-HT drugs are recommended for symptomatic patients with angina?

A

Beta blockers and CCBs

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39
Q

In patients with chronic heart failure, which specific beta blockers are recommended?

A

Carvedilol, bisoprolol (beta-1 selective antagonist), metoprolol extended release and nebivolol

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40
Q

When is low dose aspirin recommended in patients with HTN?

A

In those who have had previous CVD events (unless bleeding risk is increased)

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41
Q

Hypertension is an independent risk factor for which 5 conditions? (name at least 3)

A

MI, haemorrhagic and ischaemic stroke, CKD, heart failure and premature death

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42
Q

What are the consequences of untreated or uncontrolled hypertension?

A

Continuous increases in CVD risk, and the onset of vascular and renal damage

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43
Q

What is the definition of ‘hypertensive urgency’? What are the treatment principles?

A

Severe BP elevations (>180/110) that are not immediately life-threatening but are associated with either symptoms (i.e.. severe headache) or moderate target organ damage. Treatment with oral drugs and follow up within 24-72 hours are recommended

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44
Q

What is the definition of a ‘hypertensive emergency’? What are the treatment principles?

A

BP very high (often >220/140) and acute target organ damage or dysfunction is present (i.e., heart failure, APO, MI, aortic aneurysm, AKI, major neurological changes, hypertensive encephalopathy, papilloedema, cerebral infarction, haemorrhagic stroke). Hospitalisation, close BP monitoring and parenteral antihypertensive drug therapy are indicated.

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45
Q

What is accelerated hypertension?

A

Severe hypertension accompanied by the presence of retinal haemorrhages and exudates

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46
Q

What is malignant hypertension?

A

Severe hypertension with retinal haemorrhages and exudates plus papilloedema

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47
Q

List and describe the categories of hypertension

A 
High normal 130-139/85-89
Grade 1 (mild) 140-159/90-99; 
Grade 2 (moderate) 160-179/100-109; 
Grade 3 (severe) 180/110
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48
Q

List at least 3 signs of end organ damage in patients with hypertension

A

Renal impairment, albuminuria, cardiac hypertrophy or vascular disease

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49
Q

The BP management guidelines recommend that clinical judgement apply to patients with additional risk factors not included within the Framingham risk calculator. Name at least 3 examples of patients where the criteria underestimate the risk.

A
  1. Sedentary or obese
  2. Socially disadvantaged
  3. Increased triglycerides/fibringogen/apolipoprotein B, elevated CRP,
  4. Elevated fasting glucose
  5. FHx of premature CVD (immediate relative before age 55 men and 65 women)
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50
Q

What is the recommended method for taking BP in a patient who’s arm is too large for any cuff?

A

Use a cuff on the forearm and auscultate the radial artery

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51
Q

What patient conditions are required for accurate BP measurement in clinic?

A

Quiet environment at room temperature, sitting with legs uncrossed and relaxed for several minutes before, refrain from caffeine and smoking for 2 hours prior to measurement (home measurements, refrain for 30 mins)

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52
Q

On manual BP auscultation, record the systolic level at phase ____ Korotkoff, and diastolic level at phase ____ Korotkov

A

I, V

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53
Q

List at least 4 signs of arterial disease on examination

A

Carotid, renal, abdominal or femoral bruits
AAA
Absent femoral pulses
Radio-femoral delay

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54
Q

List the initial laboratory investigations recommended for all patients with hypertension

A
  1. Urine dip for blood
  2. Albuminuria and proteinuria
  3. Fasting glucose
  4. Lipids
  5. MBA20 and CBE for Hb
  6. ECG
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55
Q

What is the definition of proteinuria?

A

> 500 mg/day protein excretion rate

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56
Q

In which group of hypertensive patients is ABI recommended?

A

In those with risk factors for PVD, including diabetes, vascular bruit, older age, smoking (ABI is not recommended as for population screening in low risk patients).

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57
Q

An ABI of ___ is diagnostic for PVD

A

<0.9

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58
Q

In which patients with AF is rhythm controlled pursued early?

A

In those at risk of decompensated heart failure

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59
Q

AF is an independent predictor of which outcomes?

A

Stroke, heart failure, all-cause death

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60
Q

True or false? The risk of developing AF is reduced with moderate physical activity

A

True

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61
Q

What lifestyle measures have been shown to reduce the number of episodes and symptoms of AF, once diagnosed?

A

Weight loss and aerobic exercise

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62
Q

The AF guidelines recommend a target BMI of ?

A

27

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63
Q

List at least 4 risk factors and disease associations in AF

A

Obesity, HTN, T2DM (and impaired glucose tolerance), smoking, OSA, CAD, valvular heart disease, heart failure, CKD

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64
Q

List at least 3 potentially reversible precipitants for AF

A
  1. Hyperthyroidism
  2. Alcohol excess
  3. Electrolyte abnormalities
  4. Sepsis
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65
Q

What are the recommendations for screening for AF in Australia?

A

Opportunistically screen patients ages 65 and older with radial pulse palpation +/- ECG if irregular

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66
Q

List 3 medications which may be used when pursuing rhythm control in AF

A

Flecanide, Sotalol and Amiodarone

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67
Q

List at least 2 contraindications to Flecanide in patients with AF

A

LV dysfunction
CAD
Moderate LV hypertrophy

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68
Q

List at least 2 beta blockers which are often used preferentially for people with AF and clinical heart failure

A

Bisoprolol, Cavedilol and Nebivolol

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69
Q

List at least 2 classes of drugs which can be used for rate control in AF

A

Beta blockers, non-dihydropyridine CCBs (verapamil/diltiazem) and digoxin

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70
Q

List at least 5 routine investigations for newly diagnosed atrial fibrillation (asymptomatic)

A

CBE, UEC, Cal, Mg, phosphate, TSH, TOE, 24 hour holter, ECG, PSG (symptomatic)

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71
Q

List at least 4 situations in which patients with newly diagnosed AF should be referred to ED rather than being managed in the outpatient setting

A

Hypotention, AF with rapid ventricular rate >110 or if very symptomatic, signs of heart failure, presyncope or syncope, angina at rest (+/- ischaemic changes)

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72
Q

In the appropriate patient group, rhythm control medications in AF have what benefit?

A

a) relieve symptoms

b) half the risk of recurrence

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73
Q

List the 3 patient groups who are more likely to benefit from antiarrhythmic use in AF

A
  1. Physically active
  2. Have paroxysmal or persistent AF lasting short periods of time
  3. Do not have underlying significant cardiac structural changes
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74
Q

List the 4 types of AF and define them

A
  1. Paroxysmal (episodes <1 week in duration)
  2. Persistent (>1 week)
  3. Long-term persistent (>12 months)
  4. Permanent
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75
Q

What is the treatment approach for patients with permanent atrial fibrillation?

A

Focus on rate rather than rhythm control

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76
Q

Explain why early rhythm control results in better long-term resolution of AF

A

AF begets AF. A cycle of paroxysms of AF cause structural changes in atrial myocardium and increase the liklihood of further AF. Rhythm control aims to interrupt the cycle by maintaining sinus rhythm early, and is more successful the earlier it is used

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77
Q

List the situations in which rhythm control would be considered in the treatment of AF

A

In the fit patient with paroxysmal or short persistent AF without underlying cardiac disease;
In patients with cardiomyopathy secondary to AF with rapid ventricular response;
For people for whom AF may precipitate acute haemodynamic deterioration because of cardiac co-morbidities

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78
Q

For which groups of patients is catheter ablation reserved for the treatment of AF?

A

Only for symptomatic patients with paroxysmal/persistent AF who are refractory/intolerant to at least 1 rhythm control medication

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79
Q

List the variables in the CHA(2)DS(2)VA scoring system

A

CCF, Hypertension, Age >75 (2), Diabetes, Stroke or TIA (2), Vascular disease, Age >65 (1)

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80
Q

What are the recommendations for anticoagulation in patients with CHADSVA scores of 0, 1 and 2?

A

0 is not recommended
1 for consideration
>2 is recommended

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81
Q

List the variables in the HAS-BLED scoring system

A

Hypertension, Abnormal renal or liver function, Stroke, Bleeding history, Labile INRs, Eldery (>65) drugs (antiplatelets and nsaids) or alcohol

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82
Q

What is the main treatment aim in AF?

A

To achieve an appropriate heart rate (50-110) with either rate or rhythm control to minimise symptoms

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83
Q

In which patient groups can the Framingham criteria be used?

A

All adults 45 and older (35 if ATSI) without existing CVD or not already known to be at increased risk of CVD

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84
Q

What is relative risk?

A

A ratio of the rate of events occurring in the population exposed to a risk factor compared to the rate among the population not exposed to this risk factor

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85
Q

To reduce CVD risk, what is the recommended dietary advice with regard to saturated fatty acids?

A

<10% of total energy intake, replace with polyunsaturated fatty acids

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86
Q

To reduce CVD risk, what is the recommended dietary advice with regard to trans saturated fatty acids?

A

As little as possible (preferably none from processed food, and <1% of total energy intake from natural origin

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87
Q

To reduce CVD risk, what is the recommended dietary advice with regard to salt?

A

<5g per day

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88
Q

To reduce CVD risk, what is the recommended dietary advice with regard to fibre?

A

30-45g per day, preferably from whole grain products

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89
Q

To reduce CVD risk, what is the recommended dietary advice with regard to fruit and vegetables?

A

> 200g per day, or 2-3 servings

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90
Q

To reduce CVD risk, what is the recommended dietary advice with regard to fish?

A

1-2 times per week, one of which should include a fatty fish

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91
Q

To reduce CVD risk, what is the recommended dietary advice with regard to nuts?

A

30g per day (unsalted)

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92
Q

To reduce CVD risk, what is the recommended dietary advice with regard to alcohol?

A

Limit to 10 standard drinks/week, and no more than 4 on any one occasion

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93
Q

What is the most cost-effective strategy for preventing CVD?

A

Smoking cessation

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94
Q

Describe the smoking behaviour that indicates indicates nicotine dependence

A

Smoking within 30 minutes of waking;
Smoking more than 10 cigarettes/day;
Prior history of withdrawal symptoms or cravings on quit attempts

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95
Q

What pharmacotherapy is recommended in patients at very high risk of CVD who are unable to achieve their LDL goal despite maximum dose statin + ezetimibe?

A

PCSK9 inhibitors (monoclonal antibodies)

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96
Q

What constitutes ‘vascular disease’ in the CHADSVA criteria?

A

Prior MI or PVD or complete aortic atheroma or plaque on imaging

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97
Q

What are the recommendations for exercise in patients with HTN - in both the under and over-65 groups?

A

Under 65: should accumulate 150-300 minute moderate intensity, or 75-150 minutes of high intensity plus muscle strengthening twice weekly.
Over 65s: should do some form of activity regardless of how well they are and regardless of the type of activity (30 mins on most or all days).

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98
Q

List at least 4 patient groups who may require supervised physical activity

A 
Unstable angina
BP >180/110
Uncontrolled heart failure
MI within the past 3 months
Severe aortic stenosis
Resting arrhythmia
Diabetes with poor control
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99
Q

Patients should choose foods that have less than how much sodium per 100g?

A

<400mg

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100
Q

What is the relationship between dietary potassium and BP?

A

In normal renal function, increasing dietary potassium can reduce systolic BP by 4-8mmHg. Can be achieved by eating wide variety of fuits and veg, plain unsalted nuts and legumes

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101
Q

It is recommended that total dietary fat intake account for ___% of total energy intake

A

20-35%

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102
Q

How long does it take for to lower the risk of a coronary event to that of the normal population after smoking cessation?

A

2-6 years

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103
Q

What is the MOA of ACE-inhibitors?

A

Reduce the synthesis of angiotensin-2 by inhibiting the action of ACE

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104
Q

What is the MOA of ARBs?

A

Bind directly to the angiotensin-1 receptor, preventing it’s activation by angiotensin-2.

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105
Q

List some of the evidence that demonstrates that ACE and ARBs are not interchangeable, although they are equally efficacious in lowering BP and overall CV events

A

ACE-Is prevent the onset of nephropathy and reduce morality in early diabetes and are more effective in preventing coronary heart disease in patients with HTN. ARBs are better at preventing kidney failure in people with advanced diabetic nephropathy.

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106
Q

When combination BP medication is initiated, the combination of which drugs is superior?

A

The combination of ACE + CCB is superior to ACE + diuretics

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107
Q

What is the recommended guideline for starting drug treatment in patients with hypertension?

A

Start with a low dose of a first-line drug. If not well tolerated, change to another at low dose

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108
Q

What is the recommendation for patients with HT who have not reached target BP within 3 months of starting an anti-HT?

A

Add a second drug from a different class at a low dose (maximises efficacy and minimises adverse effects)

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109
Q

Assume you have a patient with HTN who commenced an anti-HT 6 months ago. At 3 months, the BP had not reached the target level and you added a second agent. It has been another 3 months and the BP is still not at target. What is the next recommended step in management?

A

Increase the dose of one of the medications (excluding thiazide) incrementally to the maximum recommended dose before increasing the dose of the other drug

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110
Q

Assume you have a patient who has been started on 2 antihypertensive medications, both of which have been up-titrated to maximum doses, but the BP is still not at target. What is the next recommended step in management?

A

Start a third drug class at low dose, assess for non-adherence and secondary causes of HT, treatment resistance due to OSA, excess alcohol, high salt intake etc. If nil found and BP still elevated, seek specialist advice

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111
Q

In what timeframe is the the maximum effect of an antiHT like to be seen?

A

4-6 weeks after commencing

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112
Q

Which combinations of anti-HT drugs should be avoided due to risk of heart block?

A

Diltiazem and beta blocker (use with care)

Veramapil plus beta blocker

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113
Q

List at least 2 compelling contraindications for ACEs or ARBs

A

Pregnancy, angioedema, hyperkalaemia, bilateral renal artery stenosis

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114
Q

List at least 3 contraindications to diuretics

A

Gout, glucose intolerance, metabolic syndrome, hypercalcaemia, hypokalaemia

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115
Q

List at least 3 contraindications for beta blockers

A

Asthma, bradycardia, AV block, uncontrolled heart failure

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116
Q

List at least 2 adverse effects of ACEi

A

Cough, hyperkalaemia (higher risk with renal impairment), renal impairment (risk increased by NSAIDs) and angioedema (can occur years after treatment)

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117
Q

List at least 3 dihydropyridine CCBs, and 2 ‘others’

A

Dihydropyridines include amlodipine, felodipine, lercanidipine and nifedipine. Others include diltiazem and verapamil

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118
Q

Describe the differences that dihydropyridine and non-dihydropyridine diuretics have on the myocardium

A

Dihydropyridines have minimal effect on myocardial contractility and cardiac conduction, whereas the non-dihydropyridine family reduce heart rate and depress cardiac contractility

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119
Q

List at least 3 electrolyte disturbances which may result from thiazide diuretic use

A

Hypokalaemia, hyponatraemia, hyperuricaemia, hyperglycaemia

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120
Q

Explain why beta blockers should be stopped slowly over >2 weeks

A

To avoid rebound hypertension and myocardial infarction

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121
Q

What is the role of hydralazine in the treatment of HTN?

A

Peripheral (mostly arteriolar) vasodilator, used for refractory hypertension, usually with a beta blocker and diuretic (the beta blocker can be used to prevent reflex tachycardia and angina

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122
Q

What are the recommendations for antihypertensives in patients who have had a stroke or TIA?

A

Any of the first line drugs are effective in reducing CVD risk, even in patients with mild hypertension

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123
Q

What is the recommendation for antihypertensives in CKD?

A

Use, as there is proven mortality benefit even in patients without hypertension

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124
Q

What should be considered if thiazide diuretics are being used in a patient with CKD?

A

Only effective in those with normal renal function or mild impairment

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125
Q

In the early phase post-MI, which drug class has been shown to reduce re-infarction in the first 2 weeks?

A

Beta blockers

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126
Q

Which antihypertensive drugs are recommended in patients who have had an MI, and when should they be used?

A

ACE + beta-blockers in all patients who can tolerate them, regardless of whether the patient is hypertensive

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127
Q

There is strong evidence for which anti-HT classes in patients who have a history of MI and who have symptomatic angina?

A

Beta blockers or calcium channel blockers

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128
Q

What is the leading risk factor the development of heart failure?

A

Hypertension

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129
Q

True or false? Patients with white coat hypertension have a comparable risk of stroke to patients with sustained hypertension?

A

True

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130
Q

What is masked hypertension?

A

Opposite of white-coat hypertension, in that BP in clinic is normal but out-of-clinic is high

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131
Q

List some of the factors which may be indicative of masked hypertension

A

Non-hypertensive patients with evidence of end-organ disease, regular heavy drinkers, smokers and patients with diabetes

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132
Q

What is white coat hypertension?

A

UNTREATED patients who have high BP in clinic but not at home

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133
Q

What is the definition of treatment-resistant hypertension?

A

SBP >140 in a patient taking 3 or more antihypertensive drugs, including a diuretic, at optimal tolerated doses

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134
Q

In which patient groups are statins recommended as primary prevention? What is the target parameter?

A

In patients without prior CVD events (primary prevention) stratified as moderate to high risk, treating to an LDL target of <2

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135
Q

In which patient groups are statins recommended as secondary prevention? What are the target parameters?

A

Coronary artery disease (target LDL <1.8)
All people who have had a TIA or ischaemic stroke
Heart failure
Diabetes (LDL <1.8)

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136
Q

In which patient group is aspirin recommended for it’s CVD benefits?

A

In patients with hypertension and previous CVD events (unless bleeding risk is increased) - i.e., for secondary prevention

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137
Q

Adults should have fasting lipids assessed every __ years, starting at age ___

A

5; 45 (or 35 for ATSI)

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138
Q

What are the recommendations for lipid lowering therapy in patients with low absolute CVD risk?

A

Provide lifestyle advice and repeat lipids every 5 years

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139
Q

What are the recommendations for lipid lowering therapy in patients with moderate absolute CVD risk?

A

Provide intensive lifestyle advice, consider pharmacotherapy if not reaching target after 6 months or if family history of premature CVD or if ethnic, repeat lipids every 2 years

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140
Q

What are the recommendations for lipid lowering therapy in patients with high absolute CVD risk?

A

Lifestyle advice and commence lipid lowering therapy (simultaneously with anti hypertensive unless contraindicated), repeat every 12 months

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141
Q

List the 5 lifestyle modifications that should be suggested for all people regardless of CVD risk

A

Encourage physical activity (aim for 30 mins/day), stop smoking, target waist measurement <94 for men and <80 for women, salt restrict <5g/day (65mmol/day) and limit alcohol

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142
Q

List some of the characteristics of statin-induced-muscle-symptoms

A

Bilateral, affecting larger muscles. Aching, soreness, tenderness, stiffness or weakness are common. Commonly occur within 4-6 weeks of starting or changing dose

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143
Q

List some patient symptoms that are less likely to be due to statin-induced muscle symptoms

A

Unilateral, diffuse and non-specific, neuropathic pain, nocturnal pain, cramping or joint pain make statin-induced symptoms less likely

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144
Q

List some characteristics that make some patients more likely to experience statin-induced-muscle symptoms

A

Older age, smaller BMI, females, food/drug interactions, previous statin side effects

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145
Q

Rather than increased CK alone, what is a more important prognosticator of whether a patient has had true statin-induced muscle symptoms?

A

If the CK drops when the statin is ceased

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146
Q

In patients with assumed statin-induced-muscle symptoms, what is the next step in management?

A 
Check CK (if less than 5 times upper limit of normal, cease statin for 2-4 weeks; if greater than 5 times or in the presence of muscle weakness, cease for 6-8 weeks). If symptoms persist, look for another cause. 
If symptoms resolve, can restart the same statin at a lower dose or try a different statin. 
Can also try alternate daily dosing or progressing to ezetimibe
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147
Q

Name the 2 long term adverse outcomes that have been linked to statin therapy

A 
Diabetes 
Haemorrhagic stroke (but the overall benefits of lowering CVD risk outweigh them)
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148
Q

Name at least 4 disorders that untreated lipid disorders can progress to

A

CVD, diabetes, NAFLD, CKD and pancreatitis

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149
Q

What are the primary uses of cholesterol in the body?

A

Cell membrane formation, bile acids and steroid hormones

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150
Q

Name at least 4 common causes of raised triglycerides

A

Sugary foods, inactivity, excess alcohol, smoking, medical conditions (diabetes, kidney and thyroid disorders), medications (thiazides, steroids, oestrogen)

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151
Q

What is the inheritance pattern of familial hypercholesterolaemia?

A

Heterozygous autosomal dominant

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152
Q

List at least 3 secondary causes of hyperlipidaemia

A

Hypothyroidism, CKD, poorly controlled diabetes, alcohol abuse and liver disease

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153
Q

Give an example of when a fibrate may be used to lower lipids

A

Used in severe hypertriglyceridaemia (triglycerides >10) to prevent pancreatitis (or when triglycerides have not reached target with statin therapy alone)

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154
Q

What is the mechanism of action of ezetimibe?

A

Inhibits cholesterol absorption from the gut

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155
Q

Patients with atherosclerotic CVD include those who have been diagnosed with which conditions? (Name at least 5)

A

STEMI, nonSTEMI, acute cerebral vascular event, stable angina, peripheral arterial disease

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156
Q

Drug therapy for the secondary prevention of atherosclerotic CVD usually consists of a combination of which 3 drug classes?

A

Statin, antiplatelet and ACEI (plus fluvax)

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157
Q

True or false? Statin therapy should be given irrespective of lipid levels in patients with established atherosclerotic CVD?

A

True. It has been shown to reduce cardiovascular mortality in these patients

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158
Q

What are the benefits of using anti-platelet drugs in patients with atherosclerotic CVD?

A

Prevent thrombosis and reduce the incidence of MI and death

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159
Q

What is the general recommendation for anti-platelet therapy in patients who have suffered acute coronary syndrome?

A

DAPT with aspirin plus P2Y12 inhibitor (clopidogrel, ticagrelor) for 12 months

160
Q

Regardless of the initial anti-platelet given, patients with atherosclerotic CVD benefit from long term therapy with which anti-platelet agents?

A

Aspirin or clopidogrel

161
Q

What is the recommendation for anti-platelet therapy in patients with stable atherosclerotic CVD if an indication for anticoagulation arises?

A

Usually stop the anti-platelet when the anticoagulant is started (if anticoagulation only needed for a finite time, anti-platelet can be restarted after). In high risk patients (recent stenting) it may be appropriate to continue the anti-platelet

162
Q

What is the recommendation for dosing of ACEI in secondary prevention of CVD

A

Benefits may be independent of BP action - aim to titration to maximum daily dose if tolerated

163
Q

True or false? Whilst beta-blocker therapy should be started immediately following ACS, routine long-term use is no longer recommended in all patients

A

True - the benefit of long term use in low-risk patients with successful revascularisation, preserved LVEF and no angina is likely to be small - consider ceasing after 12 months in these patients

164
Q

Which patient groups are more likely to benefit from long-term beta blocker therapy after ACS?

A

Those with reduced LVEF (less than 40%), or evidence of ongoing ischaemia including stable angina

165
Q

What are the 4 non-pharmacological recommendations for prevention of heart failure?

A
  1. Smoking cessation
  2. Avoiding excess alcohol
  3. Weight reduction
  4. Regular physical activity
166
Q

What are the 5 pharmacological recommendations for prevention of heart failure?

A
  1. BP and lipid lowering where appropriate
  2. Consider ACE in all patients with CVD
  3. SGLT2i recommended in T2DM and insufficient glycaemic control
  4. ACEi recommended in patients with left ventricular systolic dysfunction
  5. Consider beta blockers in patients with LV systolic dysfunction
167
Q

What causes of acute heart failure should be investigated and managed immediately?

A

ACS, hypertensive crisis, arrhythmia, mechanical catastrophe (ruptured intraventricular septum, mitral papillary muscle or LV free wall or acute valvular regurgitation) and PE

168
Q

What is the recommended treatment for patients who present in acute heart failure associated with pulmonary congestion who remain hypoxaemic and tachypnoeic despite O2 therapy?

A

Non-invasive ventilation (improved symptoms and reduces requirement for intubation)

169
Q

In which heart failure patients is ACE-i recommended?

A

In all patients with HFrEF (LVEF <40) unless contraindicated - decreased mortality and hospitalisation

170
Q

In which heart failure patients are beta blockers recommended?

A

For all patients with HFrEF (LVEF <40) once stabilised with no/minimal congestion on examination - decreases mortality and hospitalisation

171
Q

Which beta blockers are specifically indicated in HFrEF?

A

Bisoprolol, carvedilol, metoprolol (controlled or extended release) or nebivolol

172
Q

In which heart failure patients are mineralocorticoid receptor antagonists recommended?

A

In all patients with HFrEF (LVEF <40) unless contraindicated - decreased mortality and hospitalisation

173
Q

In which heart failure patients are diuretics recommended?

A

In those with clinical symptoms or signs of congestion - to improve symptoms and manage congestion

174
Q

In which heart failure patients are angiotensin receptor neprilysin inhibitors (ARNIs) recommended?

A

As a replacement for an ACEI or ARB in patients with HFrEF (LVEF <40) despite receiving maximally tolerated or target doses of other medications (with or without MRA) - decreases mortality and hospitalisation

175
Q

Why is concomitant use of ACE-i and ARNI contraindicated?

A

Because of an increased risk of angio oedema (need a 36 hour wash out window)

176
Q

In which heart failure patients is Ivabradine recommended?

A

In HFrEF (LVEF < 35) and sinus HR 70 and above who have not responded to maximal doses of other therapies

177
Q

Why is cardiac resynchronisation therapy contraindicated in heart failure patients with QRS duration < 130ms?

A

Because of lack of efficacy and possible harm

178
Q

List some of the groups of heart failure patients for which cardiac resynchronisation therapy may be considered

A

HFrEF with LVEF < 35 and WRS greater than 130ms
In sinus rhythm and on maximal other therapies
Can also be considered in patients who also have AF or high grade AV block

179
Q

List some of the groups of heart failure patients for which an ICD may be considered

A

Secondary prevention following rests, sustained VT with hemorrhagic compromise, VT associated with syncope. Primary prevention in patients at least 1 month following MI associated with LVEF < 30, or for those with HFrEF associated with IHD

180
Q

When should CABG be considered in HFrEF patients?

A

When associated with IHD and LVEF < 35 if they have correctable disease to reduce symptoms, decrease morbidity and increase long-term mortality

181
Q

Which antihypertensive drugs should be avoided in patients with HFrEF?

A

Diltiazem, verapamil and moxonidine

182
Q

What is the definition of heart failure?

A

Complex clinical syndrome with typical symptoms and signs that generally occur on exertion, but can also occur at rest. It is secondary to an abnormality of cardiac structure or function that impairs the ability of the heart to fill with blood at normal pressure or eject blood sufficient to fulfil the needs of the metabolising organs

183
Q

What is the definition of HFrEF?

A

Clinical symptoms with or without signs of heart failure and a measured LVEF of less than 40%

184
Q

What is the definition of HFpEF?

A

Clinical symptoms with or without signs of heart failure: and a measured EF of at least 40%; and objective evidence of either relevant structural heart disease or diastolic dysfunction without an alternative cause

185
Q

List at least 4 causes of pulmonary hypertension

A

Heart failure, hypertension, left-sided valvular heart disease, AF, obesity, chronic lung disease, sleep apnoea, CKD, PE

186
Q

List the 4 negative consequences of reduction in cardiac output

A
  1. Reduced end organ perfusion
  2. Activation of neurohormonal and inflammatory system (RAA, sympathetic nervous system)
  3. Cardiac remodelling (LV dilatation, fibrosis)
  4. Worsening cardiac function
187
Q

Name the 3 overarching causes of heart failure, and give at least 2 examples of each

A
  1. Myocyte damage or loss (ischaemia, viral disease, autoimmune and connective tissue disease, toxins such as alcohol or cytotoxic drugs, infiltration, metabolic abnormalities)
  2. Abnormal loading conditions (hypertension, high output states like anaemia or sepsis or volume overload as in renal failure)
  3. Arrythmias
188
Q

Which investigation is the single most useful investigation in patients with suspected heart failure?

A

Echocardiography

189
Q

Which 3 classes of drugs are known to improve survival and decrease hospitalisation in patients with HFrEF?

A

ACE/ARB, beta blockers, mineralocorticoid receptor antagonists (MRAs)

190
Q

When should an ACE be changed to an ARNI in heart failure?

A

When LVEF < 40 or despite initial medical management

191
Q

When should referral for ICDs and CRTs be made in heart failure patients?

A

HFrEF with LVEF < 35 despite optimal medical therapy

192
Q

Describe the presentation of paroxysmal AF

A

Episodes of AF lasting less than 7 days (whether they revert spontaneously or undergo DC cardioversion). If they are going to self terminate, it’s usually within the first 48 hours

193
Q

Describe the presentation of persistent AF

A

Episodes of AF lasting more than 7 days that do not self terminate

194
Q

What is long-standing AF?

A

Continuous AF lasting 1 year or longer, despite a rhythm control strategy

195
Q

What is permanent AF?

A

When the patient and treating doctor decide to accept that the patient will remain in AF and will not attempt to achieve sinus rhythm. Often a rhythm-control strategy has been unsuccessful

196
Q

List at least 5 concurrent conditions that increase the risk of developing AF

A

Heart failure, HTN, valvular heart disease, diabetes, obesity, OSA, excess alcohol use, hyperthyroidism

197
Q

What is valvular AF, and what are the implications of this?

A

Refers to AF in patients who have either moderate or severe mitral stenosis or a mechnical heart valve. These patients have increased risk of thromboembolism and need to be anti coagulated with warfarin - there is no data available to support the use of NOACs in these patients

198
Q

What are the 3 patient factors that increase the risk of bleeding while taking apixaban for AF?

A

Age 80 or more, weight 60kg or less, creatinine 133 or more (these are the same criteria for reducing the dose)

199
Q

The management strategy for acute AF depends on which 4 patient factors?

A
  1. Haemodynamic status
  2. Duration of the episode
  3. Thromboembolic risk
  4. Patient preference
200
Q

In which situation might immediate cardioversion be considered in a patient presenting with acute AF?

A

For those patients presenting with haemodynamic compromise

201
Q

Describe the management of a patient presenting with acute AF lasting less than 48 hours duration

A

May consider rhythm control, and should start anticoagulation at the time of cardioversion and continue longer term (depending on patient’s risk)

202
Q

Presume a patient has presented with acute AF of unknown duration, or of duration longer than 48 hours. When can cardioversion safely be offered?

A

As soon as left atrial thrombus has been excluded (then start anticoagulation at time of cardioversion and continue for at least 4 weeks), or if the patient has already been anti-coagulated in the preceding 3 weeks.

203
Q

What is the aim of rate control in AF?

A

To achieve a resting HR of less than 110bpm (oral therapy is usually sufficient)

204
Q

In which patients is it appropriate to use long term rate-control in the management of AF?

A

In those patients who are symptomatic or do not respond to rhythm control

205
Q

What pharmacotherapy may be used to achieve rate-control in AF if the patient is intolerant to beta blockers?

A

Diltiazem or verapamil

206
Q

Why should diltiazem and verapamil be avoided in patients with left ventricular dysfunction?

A

Because they have negative inotropic effects

207
Q

Assume you are trying to rate-control a patient in AF, but the patient is intolerant to beta blockers and is known to have left ventricular dysfunction. What is an alternative pharmacological option?

A

Amiodarone

208
Q

Why is digoxin considered a second-line drug for treatment of AF?

A

Because it does not usually control exercise-induced tachycardia

209
Q

Why is IV digoxin not recommended for urgent rate-control in AF?

A

The onset of action takes longer than 1 hour and effect does not peak for 6 hours

210
Q

True of false? Pharmacological cardioversion has a greater success rate of achieving sinus rhythm compared to DC cardioversion

A

False

211
Q

What anticoagulation should be commenced in patients who are planned to undergo cardioversion in acute AF (with duration <48 hours who are not already anticoagulated)?

A

Heparin or LMWH

212
Q

Which variables can be controlled in order to make cardioversion more effective in achieving sinus rhythm in a patient presenting with acute AF?

A

Biphasic current is better than monophasic.
Anterior-posterior pad placement is better.
Start with higher energy (150-200 joules)as this improves success rate and lessens the need for repeat shocks.

213
Q

What is the preferred pharmacological agent for cardioversion in acute AF in a patient with normal left ventricular function and no known CAD?

A

Flecanide (IV infusion)

214
Q

What is the preferred pharmacological agent for cardioversion in acute AF in a patient with left ventricular dysfunction (LVEF 40%) or CAD?

A

Amiodarone (IV infusion)

215
Q

What is ‘pill in the pocket’ cardioversion in the context of AF?

A

Refers to a single dose of oral flecanide to restore sinus rhythm in patients with acute AF, which is self-administered by the patient at home. It is used under Specialist supervision by selected patients with infrequent symptomatic episodes of AF. Best taken with an AV blocking drug to decrease the risk of conversion to flutter.

216
Q

List 3 drugs which may be used for the purpose of long-term rhythm control in AF

A

Felcanide, sotalol, amiodarone

217
Q

What should be monitored in patients taking sotalol for long-term rhythm control ion AF? In what instance should it be ceased?

A

QT interval (cease if QTc exceeds 500 milliseconds or increases more than 20% from baseline)

218
Q

When is PSG recommended for patients with AF?

A

In those with recurrent syptomatic AF

219
Q

Which 2 modifiable risk factors confer the greatest risk of development of PVD?

A

Diabetes and smoking

220
Q

What are the non-modifiable risk factors for PVD?

A

Age, male, and non-caucasian

221
Q

What is the primary approach for management of intermittent claudication

A

Conservative, with a walking exercise program, focus on good foot care and CVD risk modification. This is because IC has a favourable prognosis and rarely progresses to require revascularisation or amputation.

222
Q

What is the recommendation for anti-platelet therapy in patients with intermittent claudication?

A

Aspirin or clopidogrel to reduce the risk of CVD events. DAPT should not be used in patients with stable disease, as this has no advantage over aspirin alone and is associated with increased bleeding

223
Q

How is chronic critical limb ischaemia characterised? (aka chronic limb threatening ischaemia, CLTI)

A

Presence of ulceration or gangrene of the peripheries, or patients with proven peripheral arterial disease, or who experience persistently recurring ischaemic pain at rest requiring analgesia

224
Q

What is the treatment of choice in patients with critical limb ischaemia (CLTI) from PVD?

A

Vascular reconstruction (bypass graft, endarterectomy, endoluminal techniques)

225
Q

What are the principles for BP management in patients with chronic limb ischaemia?

A

Maintain high to normal systolic BP to assist perfusion (may involve decreasing dose of anti-HT)

226
Q

How is acute limb ischaemia defined?

A

Sudden onset of severe ischaemia wtih associated sensory and motor loss and intense pain (NB this is thought to be a different process to chronic limb ischaemia and the treatment is different)

227
Q

What are the common causes of acute limb ischaemia?

A

Thrombosis superimposed on pre-existing atherosclerosis, thromboembolism from heart, aneurysm or atheroma, thrombotic occlusion of an aneurysm, and trauma

228
Q

What is livedo reticularis?

A

A course net-like discolouration of the skin, which can be caused by cholesterol embolism

229
Q

The syndrome of cholesterol embolism (atheroembolism syndrome) is characterised by a cluster of laboratory abnormalities. Name at least 2.

A 
High ESR
Hypergammaglobulinaemia
Reduced serum complement (C3 and C4)
Eosinophilia 
Kidney failure
230
Q

Name at least 3 body systems which can be involved in atheroembolism syndrome

A

Skin, kidney, eye, brain and viscera, digital ischaemia, livedo reticularis, claudication, accelerated HTN, kidney failure, visceral ischaemia, ocular embolic symptoms, TIA and stroke

231
Q

Give at least 3 causes of atheroembolism syndrome

A

Following invasive vascular procedures, trauma, anticoagulation or fibrinolysis, or spontaneously

232
Q

What is a type 1 myocardial infarction? What is the the most common cause of this?

A

Spontaneous atherothrombotic occlusion which compromises myocardial blood flow. Most commonly secondary to coronary plaque rupture.

233
Q

What is a type 2 myocardial infarction?

A

MI secondary to ischaemic imbalance between myocardial oxygen supply and/or demand. Can arise from coronary artery spasm or embolism, arrhythmias, anaemia, respiratory failure and hypotension

234
Q

Non-ST elevation acute coronary syndromes (NSTEACS) are further divided into which 2 types?

A

NSTEMI (patients with myocardial infarction as determined by elevated cardiac bio markers) and unstable angina (patients without elevated bio markers)

235
Q

What is the management priority in STEMI?

A

Re-establish blood flow in the occluded coronary artery (reperfusion), which is achieved by percutaneous coronary intervention or fibrinolytic therapy

236
Q

What is the management priority in NSTEMI?

A

Plaque stabilisation and prevention of coronary occlusion with medical therapy and, if appropriate, revascularisation (stenting or bypass). Fibrinolytic therapy is not used in NSTEMI.

237
Q

True or false? Long term management of both STEMI and NSTEMI is similar

A

True

238
Q

List at least 5 factors which confer ‘very high risk’ of mortality and recurrent events in patients with ACS

A
  1. Haemodynamic instability
  2. Heart failure
  3. Cardiogenic shock
  4. Life threatening arrhythmia or cardiac arrest
  5. Recurrent or ongoing ischaemia (chest pain refractory to treatment)
  6. Recurrent dynamic ST segment and/or T wave changes
239
Q

List 2 factors which confer ‘high risk’ of mortality and recurrent events in patients with ACS

A
  1. Rise/fall of troponin consistent with MI

2. Dynamic ST segment and/or T wave changes with or without symptoms

240
Q

List at least 3 factors which confer ‘intermediate risk’ of mortality and recurrent events in patients with ACS

A
  1. Diabetes
  2. Renal insufficiency (eGFR <60)
  3. LFVEF <40%
  4. Prior revascularisation (PCI or CABG)
241
Q

What medication should immediately be started in ‘high’ or ‘very high’ risk STEMI patients?

A

DAPT + anticoagulation (heparin or LMWH)

242
Q

Following a STEMI, most patients benefit from a long-term combination of which 4 medications?

A
  1. Anti-platelet
  2. Statin
  3. Beta blocker
  4. ACEI
243
Q

What is the appropriate dose of aspirin to given in acute STEMI?

A

300mg for the first dose (crushed or chewed), then 100-150mg daily

244
Q

What is the difference between DAPT given for STEMI in patients planned for PCI vs fibrinolysis?

A

PCI you can choose any of the 3 options

For fibrinolysis, the choice is clopidogrel (300mg for the first dose, then 75mg daily)

245
Q

For patients presenting more than 12 hours after the onset of symptoms in a STEMI, in what conditions should reperfusion therapy be considered?

A

In those with continuing ischamia (persistent pain), viable myocardium (preservation of R waves in infarct-related ECG leads) or major complications (cardiogenic shock)

246
Q

What are the benefits of PCI over fibrinolysis in acute STEMI?

A

PCI better at reducing mortality, recurrent MI and stroke - and the benefit increases as the time between symptom onset and presentation increases

247
Q

Considering acute STEMI, if PCI is available, it should be delivered within ____ minutes of patient contact. If it cannot be delivered, fibrinolytic therapy should be given within _____ minutes of the patient arriving at the hospital.

A

90; 30

248
Q

Under what conditions is fibrinolysis for management of acute STEMI deemed to be unsuccessful?

A

If there has been 50% or less ST recovery after 60-90 minutes and/or haemodynamic instability

249
Q

List at least 4 ‘absolute’ contraindications to fibrinolysis in STEMI

A
  1. Any prior intracranial haemorrhage
  2. Known structural cerebral vascular lesion (AV malformation)
  3. Known malignant intracranial neoplasm (primary or metastatic)
  4. Ischaemic stroke within 3 months
  5. Suspected aortic dissection
  6. Active bleeding or bleeding diathesis
  7. Significant closed head or facial trauma within 3 months
250
Q

List at least 4 ‘relative’ contraindications to fibrinolysis in STEMI

A
  1. History of chronic and severe and poorly controlled HTN
  2. Severely elevated BP on presentation (180/110)
  3. Ischaemic stroke more than 3 months ago
  4. Dementia
  5. Traumatic or prolonged CPR
  6. Surgery in the past 3 weeks
  7. Internal bleeding within the past 4 weeks
  8. Non compressible vascular punctures in past 24 hours
  9. Pregnancy or within 1 week post partum
  10. Active peptic ulcer disease
  11. Current use of anticoagulants
  12. Advanced liver disease
  13. Infective endocarditis
  14. TIA in past 6 months
251
Q

Give at least 1 example of fibrinolytic therapy for STEMI

A 
Alteplase IV bolus followed by infusion
Tenectaplase bolus (given concurrently with heparin or LMWH)
252
Q

List the recommended timing of invasive management of NSTEACS, depending on their level of risk

A

Very high risk - within 2 hours of admission.
High risk - within 24 hours of admission.
Intermediate risk - within 72 hours of admission.

253
Q

What is the difference between the recommendations for antiplatelet therapy in patients with NSTEACS who are at high risk vs intermediate risk?

A

Very high and high risk patients are given DAPT (unless surgery will be soon, in which case give aspirin only), intermediate risk patients are given either aspirin or a P2Y12 inhibitor

254
Q

DAPT is usually recommended for ____ months after an ACS

A

12 months (after which aspirin is usually continued lifelong)

255
Q

When might spironolactone be started in a patient following ACS?

A

Added to ACE-I once that therapy has been stabilised in patients with left ventricular dysfunction, heart failure and diabetes

256
Q

In which group of patients following ACS should CCBs be reserved?

A

For those patients with post-MI angina and/or elevated BP not controlled by other drugs

257
Q

List at least 4 symptoms/signs of phaeochromocytoma

A

Associated with catecholamine excess - palpitations, flushing, sweating, tremor, headache, anxiety, hypertension

258
Q

What are the 2 most common aetiologies of pericarditis?

A

Idiopathic and viral

259
Q

The risk of CVD increases with elevation of which cholesterol components?

A

LDL and triglycerides (and low HDL)

260
Q

Broadly speaking, which 2 groups of patients require lipid modifying therapy (in addition to lifestyle modification)?

A

Those with established CVD, and those with high absolute CVD risk (>15% over 5 years)

261
Q

Which are the only 2 cholesterol components needed to calculate absolute CVD risk?

A

Total cholesterol and HDL

262
Q

Which component of cholesterol is the primary target of lipid modifying treatment?

A

LDL

263
Q

To assess the response to lipid modifying therapy, recheck lipid levels ___ weeks after starting or adjusting therapy

A

6 weeks

264
Q

What are the targets for LDL for primary prevention vs secondary prevention

A

Primary prevention <2. Seconday prevention < 1.8

265
Q

What are the target lipid levels for patients taking lipid modifying therapy?

A 
LDL (primary prevention <2; seconday <1.8)
HDL >1
Total cholesterol < 4
Triglycerides < 2
Non-HDL cholesterol <2.5
266
Q

List at least 3 effective dietary strategies for improving lipid levels

A
  1. Reduce saturated and transfats
  2. Replace saturated fats with monounsaturated and polyunsaturated fats
  3. Increase intake of soluble fibre
  4. Introduce plant sterol-enriched milk, margarine or cheese
  5. Limit alcohol intake
267
Q

What is the most effective dietary measure for improving lipid levels, and has been associated with reducing LDL by 10-15%?

A

Introduce plant sterol-enriched milk, margarine or cheese products to diet

268
Q

Name the 2 most effective interventions for increasing HDL levels

A

Increasing physical activity and losing weight

269
Q

What should be considered in a patient who is unable to achieve target LDL levels despite maximum dose of statin?

A

Add ezetimibe (or a PCSK9 inhibitor)

270
Q

What should be considered in a patient who is unable to achieve target LDL levels despite maximum dose of statin + ezetimibe (or PCSK9 inhibitor)?

A

Consider adding a bile acid binding resin or fenofibrate

271
Q

What should be considered in a patient who is unable to achieve target triglyceride levels despite maximum dose of statin?

A

Add fenofibrate

272
Q

Name at least 2 statins which are considered to be ‘high potency’ due to their ability to reduce LDL to a greater degree

A

Atorvastatin and rosuvastatin

273
Q

What is high-intensity statin therapy?

A

Refers to treatment of high cholesterol with a high dose of a high potency statin - this is generally used in patients in the following groups:

a) established CVD for secondary prevention
b) for primary prevention if follow up and titration is unlikely to occur
c) if LDL is particularly elevated
d) if the patient is at particularly high CVD risk

274
Q

List at least 4 factors which increase the risk of true statin intolerance

A

Preexisting muscle, liver or renal disease, high potency therapy, concurrent drugs/illness, frailty and advanced age

275
Q

List at least 4 features suggesting of true statin-related muscle symptoms

A

Bilateral pain, aching or stiffness (rather than shooting pain or cramping)
Pain located in large muscle groups
Onset 4-6 weeks after starting or increasing dose
High potency therapy
Elevated CK concentration that decreases with statin withdrawal

276
Q

If a statin is determined to be the cause of muscle symptoms, what approaches are recommended?

A

Avoid complete discontinuation - consider trial of alternate statin, low dose therapy or alternate daily dosing

277
Q

Statin therapy may continue in a patient without symptoms, provided the serum CK does not exceed _ times the upper limit of normal

A

5

278
Q

If a patient who is using a statin presents with severe myalgia, or myalgia associated with muscle weakness, which rare but life-threatening condition should be ruled out? Which 2 tests should be performed to confirm the diagnosis?

A

Rhabdomyolysis, measure serum CK and urinalysis to detect myoglobinuria

279
Q

What degree of elevation of CK is usually seen in true rhabdomyolysis?

A

10 x upper limit of normal

280
Q

Mild elevation of which liver enzyme is associated with statin therapy, but is not associated with clinically relevant liver dysfunction?

A

ALT

281
Q

Bile acid binding resins cause an increase in which cholesterol component, and thus are not suitable for patients with elevation in this marker?

A

Triglycerides

282
Q

Severely elevated triglycerides > 10 significantly increase the risk of what illness?

A

Acute pancreatitis

283
Q

Give an example of a concurrent medical condition which can cause elevated triglycerides, and whereby treatment of the underlying condition alone can improve triglycerides.

A

Poorly controlled T2DM

284
Q

In what situation would you prescribe concurrent statin therapy with fenofibrate initially?

A

For moderately elevated triglycerides >4, when there is also HDL < 1. For those with triglycerides <4, start with a statin alone as per usual

285
Q

Severely elevated triglycerides >10 should be treated with which 2 drugs in combination?

A

Fenofibrate + fish oil (2-4g omega 3 fatty acids daily)

286
Q

Why is familiar hypercholesterolaemia so significant?

A

Because it accelarates CVD by 20-40 years

287
Q

In which patients should familal hypercholesterolaemia be suspected?

A

LDL severely elevated
Tendon xanthomata
Strong family history of premature CVD events (CVD events occurring in men < 55 or women < 60)

288
Q

List at least 5 common secondary causes of dyslipidaemia

A

Hypothyroidism, nephrotic syndrome, cholestasis, poorly controlled T2DM, obesity, excessive alcohol consumption, CKD, some drugs (thiazides, beta blockers, oestrogen)

289
Q

Which component of the lipid profile is the most atherogenic component?

A

LDL

290
Q

List some of the causes of high triglyceride levels

A

Sugary foods, inactivity, excess alcohol or binge drinking, smoking, diabetes, kidney and thyroid disorders, thiazides, steroids, oestrogen and inheritance

291
Q

What is the inheritance pattern of familial hypercholesterolaemia? What percentage of first degree relatives are affected?

A

Autosomal dominant, 50% affected due to monogenic inheritance and high penetrance

292
Q

Which 3 scenarios are considered to be high risk of familial hypercholesterolaemia?

A
  1. DLCNC score
  2. LDL >6.5 in the absence of secondary causes
  3. LDL 5-6.6 with signs of premature or accelerated atherogenesis
293
Q

Describe the ECG changes seen in the various stages of pericarditis

A

Stage 1: diffuse ST elevation with PR depression and reciprocal changes in aVR (first 2 weeks).
Stage 2: resolution of stage 1 with generalised T wave flattening (1-3 weeks).
Stage 3: T wave inversion (3 to several weeks).
Stage 4: resolution (several weeks onwards)

294
Q

In a patient presenting for the first time with symptoms consistent with intermittent claudication, what is the next most appropriate investigation to perform, and what would it show?

A

Ankle brachial index <0.9

295
Q

Medical management of AAA generally involves CVD risk reduction and pharmacotherapy with which 3 classes of medication?

A

Antiplatelets, statins and antihypertensives (NB this is not to reduce the size or prevent the expansion of the aneurysm, but to improve survival at future surgical repair)

296
Q

When is surgical intervention for AAA generally recommended?

A

When AAA size > 5.5cm in men and 5cm in women

297
Q

Average home BP readings over what value is the threshold for diagnosing HT?

A

HTN diagnosed if at home readings average to 135/85 or above - NB different from in office diagnostic criteria.

298
Q

In general, drug therapy for the secondary prevention of atherosclerotic CVD usually consists of which 4 medications?

A

Antiplatelets, statin, ACE and beta blocker

299
Q

Presume a patient presents to you with a HTN and a family history of premature CVD. You order a coronary artery calcium study and the result is 150. What treatment would you recommend to this patient?

A

Aspirin + statin for primary prevention of MI

300
Q

State the most common causes of secondary hypertension in children up to the age of 11, compared to older adults > 65

A

In children, renal parenchymal disease (reflux nephropathy, GN, PCKD) and coarctation of the aorta.
In older adults, atherosclerotic renal artery stenosis and renal failure are most common.
In the intermediate age group, OSA and adrenal/endorcrine are most common (hyperaldosteronism, thyroid dysfunction, cushings syndrome, phaeochromocytoma

301
Q

List the 5 classes of medications which confer improvements in ourcomes in HFrEF

A

ACE, ARB, beta blockers, aldosterone antagonists, ARNIs

302
Q

When might an ARNI be considered in the management of HFrEF?

A

If patients are symptomatic despite maximum doses of an ACE (or ARB) and beta blocker (the ARNI is used in place of the ACE/ARB)

303
Q

What is the evidence for iron deficiency/replacement in HFrEF?

A

Strongly associated with increased mortality. IV iron improves symptoms, exercise tolerance and QOL, and may reduce hospitalisation

304
Q

ARB and ACEI therapy in heart failure require frequent monitoring of which 3 parameters?

A

Hypotension, kidney impairment and hyperkalaemia

305
Q

Presume you have a patient who takes long term atenolol, and they develop HFrEF. What should you do with regard to management with a beta blocker?

A

Switch to a beta blocker than has been shown to improve clinical outcomes in HFrEF - these are nebivolol, metoprolol, carvedilol and bisoprolol

306
Q

Explain why beta blockers can initially cause worsening of heart failure when started

A

Because they block the sympathetic activation of the failing heart

307
Q

List the 5 pieces of advice for how to reduce the risk of complications (hypotension/bradyarrythmia) when starting a beta blocker for HFrEF

A

Beta blockers are essential for these patients, and we start them even in patient groups where they would usually be avoided. To minimise adverse outcomes, do not start during acute heart failure decompensation; start at a low dose; increase the dose very gradually (double every 3-4 weeks); monitor symptoms frequently and monitor weight daily; avoid simultaneous addition of vasodilator drugs

308
Q

Beware of life threatening ______ when adding an aldesterone antagonist or potassium sparing diuretic to an ACE/ARB in patients with kidney impairment.

A

Hyperkalaemia

309
Q

HFpEF is more common in which 2 patient groups?

A

Older women and patients with high BP

310
Q

List the 4 princples of treatment for patients with HRpEF

A
  1. Diagnose and treat the cause (HTN)
  2. Identify and treat precipitating factors (i.e., AF)
  3. Treat the symptoms (diuretics)
  4. Recognise and treat comorbidities (HTN, IHD, diabetes)
311
Q

List at least 3 classes of drugs which can cause harm in patients with HFpEF

A
  1. Diuretics (usually normal left ventricular volume so excessive diuresis can lead to reduced CO and BP)
  2. Venodilators like isosorbide (reduction in CO and BP)
  3. Powerful arterial vasodilators (hydralazine - can cause left ventricular outflow obstruction)
  4. Digoxin and other inotropic drugs
312
Q

The clinical features of acute cardiogenic pulmonary oedema stem from which 2 major pathophysiological processes?

A

Intra-alveolar fluid accumulation and extreme sympathetic nervous system activation

313
Q

Describe the presentation of acute cardiogenic pulmonary oedema

A

Rapid onset severe dyspnoea (usually at night) + tachypnoea + tachycardia, may have poor peripheral perfusion, agitation and restlessness, widespread crepitations

314
Q

What is the first step in management for a patient presenting with acute cardiogenic pulmonary oedema?

A

Sit as upright as possible, arrange urgent ambulance transport if not already in hospital. Use furosemide 20-80mg IM or IV, repeated at 20 minutes if needed + high flow oxygen via mask with a reservoir (if sats <94%)

315
Q

In a patient presenting with acute cardiogenic pulmonary oedema, who has had inadequate response to IV furosemide and O2, what is the next step in management?

A

Add GTN (with caution if SBP<100 or signs of poor peripheral perfusion), 400mcg spray sublingually and repeat every 5 minutes up to max 1200mcg

316
Q

List at least 4 reversible precipitating causes of acute cardiogenic pulmonary oedema

A
  1. Hypertensive emergency
  2. MI
  3. Arrhythmia
  4. Mitral regurgitation or other acute valve dysfunction
  5. Acute PE
317
Q

In what situation could morphine IV be given for acute cardiogenic pulmonary oedema?

A

If a patient has not improved with furosemide, O2 and GTN, and the patient is not tolerating attempts at NIV. Can give 1-2.5mg IV as a single dose

318
Q

What are the indications for cardiac resynchronisation therapy (CRT) in heart failure?

A

Patients in sinus rhythm who are symptomatic despite optimal medical therapy, with EF <35% and QRS duration 0.13 seconds or more (the CRT improves the poor coordination of ventricular contraction in these patients)

319
Q

Name 3 complications of percarditis

A

Pericardial effusion, tamponade and myopericarditis

320
Q

What clinical findings are characteristic of cardiac tamponade?

A

Decreased BP, elevated JVP, muffled heart sounds (Beck’s Triad) and pulsus paradoxus

321
Q

In what position is a pericardial rub best heard?

A

With the patient leaning forward, in expiration, heard over the left lower sternal border

322
Q

For how long should patients with acute pericarditis avoid strenuous exercise?

A

Until symptom resolution, or for at least 3 months in competitive athletes

323
Q

Which patient groups with pericarditis should be considered for concomitant PPI use for gastric protection from NSAIDs and colchicine?

A

Over 65, prior history of GI ulcer, those taking concurrent aspirin, steroids or anticoagulants

324
Q

The development of cardiac tamponade in acute pericarditis is based on what factor?

A

On the rate of fluid accumulated in the pericardium (rather than the quantity). Pericardial effusion is common, but progression to tamponade is rare

325
Q

What is Kussmaul sign?

A

A paradoxical rise in JVP on inspiration

326
Q

What is considered first line treatment for acute pericarditis?

A

Combination of NSAID for 7-10 days, plus colchecine for 3 months (with PPI for patients at high risk of GI toxicity)

327
Q

All patients with suspected pericarditis should have which 5 tests (if available)?

A

ECG, CXR, inflammatory markers, troponin, echo (to confirm the diagnosis and any complications, and to rule out other life threatening causes of chest pain)

328
Q

Give some examples of indications for hospital admission in patients presenting with pericarditis

A

If a specific treatable cause is identified, or if one of the following risk factors for poor prognosis is present:
high fever 38
subacute onset over several days
large pericardial effusion
cardiac tamponade
failure to respond within 7 days to aspirin or nsaids

329
Q

List at least 4 indications for screening of primary aldosteronism

A
  1. Sustained BP above 150/100 on each of 3 measurements on different days;
  2. HT >140/90 despite 3 antihypertensives;
  3. Controlled BP < 140/90 on 4 or more antihypertensives;
  4. HTN and spontaneous or diuretic induced hypokalaemia;
  5. HTN and adrenal lesion;
  6. HTN and OSA;
  7. HTN and FHx of early onset HTN or CVA younger than 40 years of age;
  8. All hypertensive first degree relatives of a patient with primary aldosteronism
330
Q

What is the most common specifically treatable and potentially curable cause of hypertension?

A

Primary hyperaldosteronism (Conn’s syndrome)

331
Q

Why is the diagnosis of Conn’s syndrome so important as a cause of secondary hypertension?

A

Because it carries a much higher risk of adverse CVD outcomes than essential hypertension, as aldosterone alone has been shown to cause cardiovascular inflammation, fibrosis and remodelling

332
Q

What is an appropriate screening test of primary aldosteronism? What result signifies a positive test?

A

aldosterone to renin ration 2 hours after rising in the morning (does not need to be fasting). If ARR > 70, the test is positive

333
Q

Which groups of patients should be considered for coronary calcium scores?

A

Patients aged 45-75 with intermediate CVD risk (and asymptomatic), or for lower risk patients with concerning features not included in the Framingham risk calculator (i.e., strong family history of premature CAD or diabetes in people aged 40-60)

334
Q

Studies have shown that prophylactic aspirin + statins in the primary prevention of CVD have net benefit amongst people with a coronary calcium score of ___?

A

> 100

335
Q

Which patient groups with AF should be treated with warfarin instead of a NOAC?

A

Those with mdoerate-severe mitral valve stenosis or a metallic valve replacement (i.e., ‘valvular AF’)

336
Q

Name 4 absolute contraindications for anticoagulation in AF

A
  1. Severe renal impairment (CrCl < 15 for apixaban)
  2. Liver cirrhosis
  3. Current active bleeding or coagulopathy
  4. Previous life threatening haemorrhage whilst on an anticoagulant
  5. Anaphylaxis to the anticoagulant
337
Q

What are the criteria for renal adjustment of Apixaban?

A

At least 2 of: creatinine >133; Age > 80; weight < 60 (these are also the factors that increase bleeding risk)

338
Q

How do you swap from warfarin to a NOAC?

A

Cease warfarin and start NOAC when the INR is less than 2

339
Q

What is the advice for anticoagulation in patients with AF who also have IHD and who undergo PCI?

A

Triple therapy with aspirin, clopidogrel and anticoagulation (no longer than 6 months post PCI).
Then continue dual therapy with clopidogrel and anticoagulation for at least 12 months after PCI before considering stopping antiplatelet therapy and continuing anticogulation as monotherapy

340
Q

What is the target weight loss/BMI for patients with AF?

A

Loss of 10% body weight with target BMI < 27

341
Q

What is the recommendation for alcohol intake in patients with AF?

A

No more than 3 standard drinks/week

342
Q

Which patient groups with AF can be considered for catheter ablation?

A

Those with paroxysmal and persistent AF who are symptomatic, and those with left ventricular dysfunction

343
Q

The treatment of AF consists of which 3 components?

A
  1. Reduction of thromboembolic risk
  2. Symptom relief (rate or rhythm control)
  3. Treatment of associated comorbidities
344
Q

In general terms, when is rate vs rhythm control used most often in newly diagnosed AF?

A

Rate control reasonable in patients who are asymptomatic and have normal left ventricular function. Rhythm control is reasonable in patients who are highly symptomatic, or who have left ventricular dysfunction that might be secondary to AF

345
Q

If considering rhythm control in a patient presenting with AF lasting less than 48 hours, how should their anticoagulation be managed?

A

Given at the time of cardioversion and continued longer term, depending on the patient’s thromboembolic risk. Specifically, LMWH or UF should be given to women with a CHADSVASC of 1 or more, and men with a score of 2 or more

346
Q

If AF has persisted for longer than 48 hours (or if the duration is unknown), acute cardioversion should not be attempted unless 1 of which 2 conditions are met?

A
  1. Left atrial thrombus has been excluded with TOE;

2. The patient has been anticoagulated for the previous 3 weeks

347
Q

The aim of rate control in AF is to achieve a resting HR of < ____bpm

A

110

348
Q

Give at least 1 example of a drug that can be used to maintain longterm rhythm control in AF, in a patient who has not tolerated a beta blocker, or in whom it is contraindicated

A

Diltiazem MR or Verapamil MR 180mg daily (but cannot be use in HFrEF, so amiodarone may be used instead)

349
Q

For a patient with AF with normal LV function and no CAD, which is the pharmacological antiarrythmic of choice for cardioversion?

A

Flecanide by IV infusion

350
Q

For a patient with AF with EF < 40% or CAD, which is the pharmacological antiarrythmic of choice for cardioversion?

A

Amiodarone 300mg by IV infusion

351
Q

Describe a pharmacotherapy regimen for maintaining long term rhythm control in AF

A

Flecanide PO 50mg BD.
Should be used in conjunction with an AV nodal blocking drug to reduce the risk of conversion to flutter - i.e., with sotalol 40mg BD

352
Q

List at least 4 ECG findings in hyperkalaemia

A 
Peaked T waves
Prolonged PR segments
Loss of P waves
Bradycardia
Sine wave
353
Q

In any patient who has suffered a bradycardia PEA arrest, suspect and treat for which reversible cause?

A

Hyperkalaemia

354
Q

Name 2 common causes of pseudohyperkalaemia

A

Delayed transfer of sample to lab
Haemolysis (can be caused by cooling or turbulent collection)
Thrombocytosis

355
Q

Define mild, moderate and severe hyperkalaemia

A

mild 5.3 - 6;
moderate 6 - 6.9;
severe 7+

356
Q

What are the 2 most common causes of hyperkalaemia?

A

Most common is chronic kidney disease (reduced K+ excretion), followed by depleted fluid volume (reduced K+ excretion secondary to reduced distal tubular water and sodium delivery)

357
Q

Give at least 3 examples of conditions which can cause hyperkalaemia via increased K+ release from cells

A

metabolic acidosis
insulin deficiency
tissue damage
rhabdomyolysis

358
Q

What is the MOA of calcium channel blockers?

A

Block inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system. Act on coronary arteriolar smooth muscle to reduce vascular resistance and myocardial O2 requirements, relieving angina symptoms.

359
Q

What is the difference between dihydropyridine and non-dihydropyridine CCBs?

A

Dihydropyridines act mainly on arteriolar smooth myscle to reduce peripheral vascular resistance on MP. Non-dihydropyridines (diltizaem and verapamil) act on cardiac and arteriorlar smooth muscle. They reduce cardiac contractility, heart rate and conduction

360
Q

For how long should aspirin be continued following insertion of any type of cardiac stent?

A

Indefinitely

361
Q

In what situations is ‘triple therapy’ with DAPT + anticoagulation indicated?

A

Sometimes in patients who have had a cardiac intervention and also an indication for anticoagulation (e.g., a patient who has had PCI and also has AF)

362
Q

What are the ECG features of an inferior STEMI?

A

ST elevation in leads II, III and aVF, and reciprocal depression in aVL + progressive development of Q waves in II, III and aVF

363
Q

Inferior STEMI can result from occlusion of which 3 arteries?

A

Any of the 3 main coronaries.
Most commonly the right coronary artery, but can also be the left circumflex or occasionally a wraparound from the left anterior descending

364
Q

In patients with diabetes and CVD risk, what are the benefits of SGLT2i?

A

Reduce CV events and decrease risk of hospitalisation for heart failure

365
Q

Name at least 5 conditions which can preipitate acute heart failure, and which should be diagnosed and treated immediately

A

ACS, hypertensive crisis, arrhythmia, mechanical catastrophe, PE

366
Q

Oxygen therapy is recommended in patients with acute heart failure with when sats are < ?

A

94%

367
Q

Name and describe the 2 types of amiodarone-induced thyrotoxicosis

A

Type 1 - related to the high iodine content of amiodarone (treated with antithyroid drugs)
Type 2 - direct damage to thyroid cells (treated with high dose steroids)

368
Q

True or false? The aim of medical management of AAA is to limit expansion and reduce the size of the AAA

A

False - the purpose is to improve overall mortality and outcomes in future AAA repair

369
Q

What are the implications of AAA on driving in Australia?

A

Untreated atherosclerotic aneurysms > 5.5cm disqualify patients from an unconditional licence except with the approval of a treating vascular surgeon

370
Q

All patients with AAA should also be screened for ___ at the time of diagnosis. What imaging is recommended?

A

TAA - with plain XR in 2 planes or non-contrast CT

371
Q

List at least 2 examples of when screening for AAA may be considered

A

In male patients > 65 with history of smoking
Patients aged > 65 with primary relative with AAA
Adult patients with personal or primary family history of connective tissue/collagen disease
Patients with known popliteal aneurysm or TAA

372
Q

What are the most effective forms of pharmacotherapy for smoking cessation?

A

Varenicline or combined NRT (patch + short acting oral form)

373
Q

What is the most common adverse effect associated with Varenicline?

A

Nausea

374
Q

Patients with atherosclerotic disease include those who have been diagnosed with which 5 conditions?

A

STEMI, non-ST elevation acute coronary syndrome (NSTEACS), acute CVA, stable angina, peripheral arterial disease

375
Q

Drug therapy for the secondary prevention of atherosclerotic CVD usually consists of a combination of which medications?

A

Antiplatelets, ACE-I, statin (high intensity regardless of lipid levels) and regular fluvax

376
Q

What is the current (2022) advice with regard to beta blocker therapy in secondary prevention of atherosclerotic CVD?

A

Should be commenced immediately following ACS, but routine long-term use is no longer recommended in all patients. The benefit of long term beta blocker therapy in low risk patients with successful revascularisation, preserved LV function and no angina is likely to be small - consider stopping after 12 months in these patients

377
Q

How is PAD classified?

A

Using the Rutherford or Fontaine classification as asymptomatic, intermittent claudication or critical limb ischaemia (now called chronic limb threatening ischaemia) - (based on symptoms, signs, ABI etc)

378
Q

Chronic limb threatening ischaemia (CLTI) presents in what clinical way?

A

With either rest pain (worse when the limb is elevated or at night), and tissue loss (gangrene, ulceration, necrosis)

379
Q

What significant finding is indicative of PAD on lower limb duplex US

A

Stenosis > 75%

380
Q

In what situation is CT angiography indicated in PAD?

A

Second-line after duplex US when concerns about aorto-iliac disease arise following US, or for operative planning

381
Q

What is the BP target in patients with HTN and PAD?

A

<140/80

382
Q

When commencing statin therapy for patients with PAD, what are the treatment targets?

A

Lower LDL to < 1.8, or decrease by 50% if baseline is 1.8-3.5

383
Q

What are the requirements for home BP measurements?

A

Take after 5 minutes of rest, 2 readings 1 minute apart. Take seated, at rest, before medication, food or exercise. Record for 5-7 days BD. Abstain from caffeine and smoking 30 minutes prior to recording

384
Q

Explain why ACE and ARBS are the superior choice for first line antihypertensive treatment in patients with T2DM

A

Because they slow the progression to microalbuminuria and reduce the risk of renal impairment

385
Q

What is the rationale for using DAPT in ACS?

A

For the prevention of stent thrombosis

386
Q

What is the mechanism of action of aspirin vs the other antiplatelets agents?

A

Aspirin irreversibly inhibits COX-1 (and hence production of thromboxane A2 which usually promotes platelet aggregation - platelet function not restored until new platelets made in 7-10 days) whereas clopidogrel/prasugrel and ticagrelor are ADP receptor antagonists (stop the fibrin linking and platelets clumping)

387
Q

How long before surgery is it recommended for clopidogrel to be ceased? What about aspirin?

A

Clopidogrel 5 days (and recommence as soon as it is safe to do so). Aspirin 7-10 days

388
Q

How many ventricular ectopics in 24 hours is considered ‘normal’?

A

Up to 100

389
Q

Explain why polyuria may present with AF

A

Due to associated release of atrial natriuretic peptide

390
Q

Patients with symptomatic coronary artery stenosis should be commenced on _____ therapy and considered for surgery

A

antiplatelet

391
Q

Patients with asymptomatic coronary artery stenosis should be commenced on best medical therapy (antiplatelets, statin and CVD risk modification) and referred to a vascular surgery service when the degree of stenosis exceeds what value?

A

> 80%

392
Q

What is dumping syndrome?

A

In the realm of bariatric surgery - syndrome caused by rapid emptying of the stomach, presenting with abdominal pain, diarrhoea, nausea, flushing, sweating, palpitations, agitation and syncope after meals rich in carbohydrates

393
Q

List at least 3 symptoms which may suggest that adjustment of a gastric band is required in patient who has had bariatric surgery

A

GORD, vomiting, regurgitation, chronic cough, recurrent aspiration pneumonia

394
Q

List at least 5 contraindications to Phentermine in weight loss management

A

CVD, anxiety, hyperthyroidism, history of drug or alcohol dependence, concomitant treatment with MAOIs, pregnancy and breastfeeding

395
Q

List the 2 serious adverse effects associated with GLP1 RAs for weight loss that patients should be counselled about

A

Pancreatitis and symptomatic gallstones

396
Q

True or false? Semaglutide must be prescribed in caution for weight loss in patients without diabetes, as there is a risk of hypoglycaemia

A

False - semaglutide does not cause hypoglycaemia in non-diabetic patients because GLP-1 requires elevation of glucose concentrations to stimulate insulin secretion

GP (4 decks)

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