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Year 3 > Block 31 Week 2 > Flashcards

Block 31 Week 2 Flashcards

1
Q

what is angina?

A
  • Angina refers to thecentral pressing, squeezing, or constricting chest discomfortthat is experienced when there is a reduction in blood flow through the coronary arteries
  • There may be typical radiation to the arm, jaw or neck and it is bought on by physical or emotional exertion and relieved by rest.
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2
Q

angina typically lasts?

A

less than 10 minutes

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3
Q

People with angina secondary to CAD are at risk of a major cardiac event:

A
  • MI
  • cardiac arrest
  • death
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4
Q

stable angina?

A
  • pain with physical or emotional exertion
  • that lasts less than 10 mins
  • should be relived within minutes of rest or with the use of medication (e.g. GTN spray).
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5
Q

UA?

A
  • sudden new onset angina
  • or sig or abrupt deterioration in angina that has been stable
  • This typically relates to pain that increases with frequency and severity or pain that is experienced at rest
  • urgent admission required for ACS exclusion
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6
Q

Aetiology of angina?

A
  • most commonly due to CAD - atheroscleortic plaques in coronary vessels
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7
Q

angina RF?

A
  • High cholesterol
  • Hypertension
  • Smoking
  • Diabetes
  • Obesity
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8
Q

Non mod RF for angina?

A
  • age
  • FHx
  • male sex
  • premature menopause
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9
Q

other causes of angina - prinzmetal?

A
  • Coronary artery spasm(Prinzmetal angina)
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10
Q

other causes of angina - microvascular?

A
  • Microvascular angina(diffuse vascular disease within the microvasculature of the coronary circulation)
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11
Q

Other causes of angina - vasculitis?

A

(e.g. Kawasaki disease, polyarteritis nodosa)

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12
Q

other causes of angina - mismatch?

A

(oxygen supply/demand mismatch)

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13
Q

other causes of angina - severe?

A
  • Severe left ventricular hypertrophy(reduced subendocardial blood flow and increased susceptibility to ischaemia)
  • Severe aortic stenosis(increases myocardial oxygen demand)
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14
Q

Chronic CS

A
  • results from atherosclerotic obstruction of coronary vessels
  • may present in different ways: ACS or CCS
  • symptomatic CAD without ACS
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15
Q

CFs of angina - 3 classical?

A
  • Constricting pain experienced in the chest +/- typical radiation to the arm/neck/jaw
  • Precipitated by physical exertion
  • Relieved by rest or GTN within 5 minutes
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16
Q

non anginal chest pain?

A

≤1 of the above features

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17
Q

grading angina?

A
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18
Q

Factors that make the chest pain more likely to be non-anginal?

A
  • Continuous or very prolonged pain, and/or
  • Unrelated to activity, and/or
  • Bought on by breathing, and/or
  • Associated with dizziness, palpitations, paraesthesia
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19
Q
A
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20
Q

other features of angina?

A
  • dyspnoea
  • palpitations
  • syncope
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21
Q

dysponea?

A

may be the only presenting feature of CAD in the absence of chest pain - consider CAD if made worse by exertion and improved on rest

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22
Q

palpitations?

A
  • Palpitations - angina may be precipitated by tachyarrhythmias (e.g. atrial fibrillation).
  • These increase the oxygen supply/demand mismatch and reduce the filling time of the coronary vessels during diastole.
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23
Q

syncope with angina?

A
  • syncope - may be suggestive of dangerous valvular or cardiac muscle disease causing angina, particularly if it occurs on exertion.
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24
Q

Chest pain suggestive of ACS?

A
  • Chest pain lasts > 10 minutes
  • Chest pain not relieved by two doses of GTN taken 5 minutes apart
  • Significant worsening/deterioration in angina(e.g. increased frequency, severity or occurring at rest)
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25
Q

how is angina graded?

A
  • Canadian Cardiovascular Society
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26
Q

Diagnostic work-up of angina?

A
  • required for patients w suspected angina or recent onset chest pain
  • excludes posibility of ACS
  • basic investigations - blood tests, ECG, echo, +/- chest X ray
  • CAD probaibility
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27
Q

rapid access chest pain clinic?

A
  • new onset angina
  • aims to identify new CAD and prevent a major cardiac event by offering earlier intervention.
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28
Q

basic Ix of angina - CAD?

A
  • determining if patients haveevidence of CADormajor risk factors for CAD(e.g diabetes mellitus).
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29
Q

Ix of angina - blood tests?

A
  • blood tests - FBC, U&Es, Lipid profile, blood glucose, HbA1c (TFTs if concern re. thyroid disease)
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30
Q

Angina ECG?

A
  • resting ECG - look for indirect signs of CAD (e.g. pathological q waves, conduction abnormalities, ST-T wave changes).
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31
Q

Echo for angina?

A
  • echo - assess LV function, valvular pathology and any motion abnormalities (sign of ischaemic disease
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32
Q

CXR of angina?

A

may be needed if atypical symptoms, features of heart failure or suspicion of pulmonary disease.

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33
Q

diagnostic testing for angina?

A
  • CT coronary angiography
  • if low likelihood of CAD
  • no history of CAD
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34
Q

stress echo for angina?

A
  • high likelihood of CAD
  • revascularisation therapy
  • established CAD
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35
Q

invasive coronary angiography for angina?

A
  • high likelihood of CAD and symptoms unresponsive to therapy
  • Typical angina at low activity level and high risk of cardiac event
  • LV dysfunction on ECHO suspected secondary to CAD
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36
Q

anatomical testing for angina?

A
  • CTA - visualisation of coronary artery lumens
  • low risk patients, excludes CAD
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37
Q

functional testing for angina?

A
  • used to diagnose obstructive CAD by detection of myocardial I
  • high likelihood of CAD
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38
Q

what are the functional tests for angina?

A
  • Dobutamine stress echocardiography
  • Stress or contrast cardiac MRI
  • Perfusion changes by single-photon emission CT(SPECT)
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39
Q

the invasive investigations for angina?

A
  • diagnose and treat obstructive CAD
  • first line for:
  • High clinical likelihood of CAD and symptoms unresponsive to medical therapy
  • Typical angina at low activity level and high risk of cardiac event
  • LV dysfunction on ECHO suspected secondary to CAD
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40
Q

management of angina?

A
  • lifestyle: diet, alcohol, smoking, excerise, weight reduction
  • Tx of comorbidities - hypertension, hypercholesterolaemia, diabetes mellitus
  • aspirin and statin prescribed
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41
Q

which drugs are those w angina put on?

A

aspirin and statins

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42
Q

Angina: GTN?

A
  • GTN - causes vascular SM relaxation and improves coronary BF
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43
Q

Side effects of GTN?

A

headache and dizziness due to low BP

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44
Q

How should GTN be used?

A
  • Patients should be advised to spray 1 to 2 doses under the tongue for an attack of angina.
  • If pain has not subsided in 5 minutes they should repeat the dose.
  • If the pain is ongoing after 10 minutes they should call for an ambulance.
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45
Q

Pharm management of angina?

A

1) BB or CCB
2) OR long acting nitrate, ivababraine, nicrorandil, ranolazine

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46
Q

Which CCB is commonly used for angina?

A

amlodepine

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47
Q

which CCBs are contra-indicated in angina?

A
  • Non-dihydropyridine calcium channel blockers, such as verapamil or diltiazem, arecontraindicated with beta-blockersdue to the risk of atrioventricular block (i.e. heart block).
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48
Q

BB + usually amlodepine for angina -

A
  • Occasionally they may be used in angina treatment as monotherapy. They should be avoided in heart failure.
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49
Q

2) if patients can’t take BBs or CCBs then monotherapy with:

Angina

A
  • long acting nitrate
  • ivabradine
  • nicorandil
  • ranolazine
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50
Q

long acting nitrate?

A

(e.g. isosorbide mononitrate): relaxation of vascular smooth muscle and increases coronary blood flow

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51
Q

ivabradine?

A

lowers heart rate through inhibition of cardiac ‘funny channels’

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52
Q

Nicorandil?

A

potassium channel agonist, which inhibits voltage-gated calcium channels leading to muscle relaxation

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53
Q

Ranolazine?

A

inhibition of late inward sodium channel, which reduces calcium overload in cardiomyocytes.

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54
Q

invasive management of angina?

A
  • revascularisation therapy in high risk patients
  • in combination with pharm therapy
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55
Q

revascularisation - the 2 options are?

A

PCI or CABG

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56
Q

PCI for angina?

A
  • Stent inserted into CA to improve coronary blood flow
  • Following a stent insertion for ‘stable’ angina,dual anti-platelet therapy should be offered for a minimum of 6 months(e.g. aspirin and clopidogrel).
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57
Q

CABG?

A
  • Coronary artery bypass grafting is a cardiothoracic surgical procedure that aims torestore flow within a coronary vesselthrough bypass of the obstructed segment.
  • This usually involves using vein grafts or redirecting flow from the internal mammary artery.
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58
Q

risk stratification for MI?

A
  • risk stratification to determine need for revascularisation therapy
  • High risk: >3% annual risk of cardiac mortality
  • Low risk: <1% annual risk of cardiac mortality
  • may be based on CAD or SCORE scores
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59
Q

revasularisation for stable angina?

A

revascularisation for those who’s symptoms aren’t being controlled well

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60
Q

STEMI revasc?

A
  • STEMI: reperfusion therapy delivered ASAP
  • coronary angiohgraphy w follow on PCI if indicated is preferred of the person peresents within 12 hours of onset of symptoms
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61
Q

unstable angina and NSTEMI revasc?

A
  • unstable angina and NSTEMI: coronary angiography
  • for those w intermediate ot higher risk of advserse CV events
  • performed ASAP for those clinically unstable or at high ischaemic risk
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62
Q

periprocedural risks of PCI?

A
  • for PCI, there’s an increased risk of platelet aggregation and thrombus formation which can lead to periprocedural ischaemic events like MI or stent thrombosis
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63
Q

Anti-thrombotics after PCI?

A
  • antithrombotis: aspirin and either clopidogrel, prasugrel, or ticagrelor
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64
Q

Which drugs are preferred over clopidoregl in UA/ NSTEMI?

A
  • prasugrel or ticagrelor are perferred over clopirogrel in unstable ngina/ NSTEMI or STEMI who are undergoing PCI as they’re faster acting
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65
Q

Benefits of revasc?

A
  • Decrease in risk of major cardiac events
  • reduced mortality
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66
Q

cardiac rehab involves?

A
  • Helps u recover and get back to as full a life as possible after a heart attack, heart surgery or following a diagnosis such as heart failure
  • individualised exercise, education and support programme built around your personal circumstances and needs.
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67
Q

Cardiac rehab - resources?

A
  • cardiac rehab - video calls, websites, telephone support
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68
Q

cardiac rehab -RF?

A
  • risk factors - eating healthy, stopping smoking, building exercise
  • exercise sessions - tailored to need and ability
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69
Q

Cardiac rehab - info and support?

A
  • information and education sessions - eating healthy, abt medications, smokingc cessation etc
  • peer support - meet people in the same situation
  • emotional support and wellbeing
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70
Q

what can cardiac rehab help w?

A
  • recovering from surgery, procedure or heart attack
  • reducing risk of further heart probs
  • improving MH
  • making lifestyle changes
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71
Q

women w CHD have ? outcomes?

A
  • women w CHD have worse outcomes than males
  • Women tend to present with coronary artery disease later in life
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72
Q

how do women w CHD present?

A
  • Women experience longer delays in access to hospital care and are less likely than men to have invasive diagnostic procedures
  • fewer women present with classical symptoms of chest pain
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73
Q

why are women’s symptoms often not recognised?

A
  • The historic limited interpretation of women’s symptoms based on the traditional approaches such as the Diamond and Forrester risk model results from under-recognition of the sex-specific presentation of IHD and contributes to misdiagnosis and delayed recognition of ischemia
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74
Q

women w IHD use more?

A
  • women with IHD use more cardiac resources and incur greater healthcare costs bc of greater symptom burdern and hospitalization
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75
Q

subgroups of women who experience worse outcomes?

A
  • Subgroups of women who experience worse outcomes for IHD include younger women (aged <55 years) and those of Black, Latino, and South Asian descent
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76
Q

south asian MI risk?

A

upto 30% more likely

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77
Q

black people MI risk?

A
  • Black people were at 51% lower risk of myocardial infarction
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78
Q

mortality from IHD in both SA men and women?

A
  • mortality from IHD in both South Asian men and women is 1.5 times that of the general population
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79
Q

which conditions do you tend to get increased TLC in?

A

asthma and COPD due to hyperinflation and less air being exhaled

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80
Q

when is the prev of HTN higher in women?

A

before 60, equal after this point

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81
Q

what is HTN a RF for?

A
  • major risk factor for myocardial infarction (MI), stroke and chronic kidney disease (CKD).
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82
Q

primary causes of hypertension?

A
  • 95%
  • no identifiable cause
  • essential or idiopathic HTN
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83
Q

secondary causes of HTN - endocrine?

A
  • primary aldosteronism
  • phaechromocytoma
  • cushings syndrome
  • acromegaly
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84
Q

secondary causes of HTN - renal?

A
  • Renovascular disease (e.g. atheromatous, fibromuscular dysplasia)
  • Intrinsic renal disease (e.g. CKD, AKI, glomerulonephritis)
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85
Q

drugs causing HTN?

A
  • Glucocorticoids
  • Oral contraceptives
  • SSRIs
  • NSAIDs
  • EPO
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86
Q

Causes of HTN to consider in younger patients?

A
  • Coarctation of the aorta(consider in children / young adults with hypertension).
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87
Q

CFs of HTN?

A
  • typically asymptomatic
  • signs and symptoms may reflect end organ damage or a potential secondary cause
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88
Q

Symptoms of HTN?

A
  • palpitations
  • angina
  • headaches
  • blurred vision
  • new neurology (e.g. limb weakness, paraesthesia)
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89
Q

Signs of HTN?

A
  • New neurology(e.g. limb weakness, paraesthesia)
  • Retinopathy
  • Cardiomegaly
  • Arrhythmias
  • Proteinuria
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90
Q

How is hypertensive retinopathy graded?

A
  • Keith-Wagener Barker (KWB) grades
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91
Q

In the following HTN patientsunderlying causes should be thoroughly excluded:

A
  • Age < 40 years
  • Reduced eGFR(suggestive of renal disease)
  • Proteinuria or haematuria(suggestive of renal disease)
  • Hypokalaemia and hypernatraemia(suggestive of Conn’s syndrome)
  • Hypertension that issudden onset, variable or worsening.
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92
Q

Bloods to do for HTN?

A
  • FBC
  • U&Es
  • Fasting glucose
  • Cholesterol(CVS risk)
  • HbA1c
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93
Q

Tests for HTN?

A
  • BP
  • urinanalysis
  • uPCR
  • ECG
  • opthalmoscopy
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94
Q

special tests for HTN?

A
  • Ambulatory BP monitoring(ABPM or HBPM)
  • Renal USS
  • Endocrine tests
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95
Q

Diagnosis of HTN?

A
  • ABPM measurements for the diagnosis of stage 1& 2 HTN
  • If clinic BP is140/90 mmHg or higher, ABPM is used to confirm the diagnosis (except in Stage 3 hypertension, in which immediate treatment is initiated).
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96
Q

ABPM?

A
  • With ABPM, at least two measurements an hour are taken during the patient’s usual waking hours (e.g. 8 am - 10 pm).
  • The average value of these measurements is used to confirm the diagnosis.
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97
Q

HBPM?

A
  • This involves taking two measurements a day (morning & evening) over a period of at least 4 days, ideally 7.
  • At each recording, two consecutive measurements should be taken at least 1 minute apart when the person is seated.
  • The readings on the first day are discarded and the average of the following readings are used to confirm a diagnosis of hypertension.
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98
Q

white coat hypertension?

A
  • ABPM monitoring prior to diagnosis of hypertension unless BP is dangerously evelated - i.e. stage 3
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99
Q

stage 1 hypertension?

A
  • ABPM > 135/85
  • Or clinic >140/90
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100
Q

stage 2 HTN?

A
  • ABPM >150/95
  • Clinic > 160/100
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101
Q

stage 3 HTN?

A

> 180/120

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102
Q

HTN staging

A
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103
Q

Mx of HTN - modifiable RFs?

A
  • discourage excessive caffeiene and alcohol
  • smoking cessation
  • consider need for anti-platelets or statins
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104
Q

who to treat for HTB

A
  • If clinic BP < 140/90 mmHg or ABPM < 135/85 mmHg, check BP at least every 5 years or more often if clinic BP close to 140/90 mmHg.
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105
Q

Features of accelerated HTN?

A
  • New onset confusion
  • Chest pain
  • Signs of heart failure(e.g. shortness of breath, fluid overload)
  • Acute kidney injury
  • Papilloedema
  • Retinal haemorrhage
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106
Q

Tx of HTN patients with T2DM or under 55?

A
  • 1) ACEi/ ARB
  • 2) add CCB or thiazide
  • 3) A + CCB + thiazide
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107
Q

first line for white patients under 55?

A

ACEi

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108
Q

first line for white patients over 55?

A

CCB

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109
Q

first line for caribbean patients?

A

CCBs

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110
Q

Tx for HTN - Age over 55 or black or caribbean origin?

A
  • 1) CCB
  • 2) add ARB/ ACEi/ thiazide
  • 3 A + CCB + thiazide
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111
Q

What can be used instead of an ACEi?

A

f patients do not tolerate an ACE-inhibitor (e.g. dry cough), offer an ARB. A combination of ACE-inhibitor and ARB should NOT be used to manage hypertension.

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112
Q
A
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113
Q
A
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114
Q
A
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115
Q

malignant/ accelerated HTN?

A

A BP >180/120 with signs of papilloedema and/or retinal haemorrhage.

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116
Q
A
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117
Q

Tx of malignant HTN aims to?

A
  • Tx attempts to reduce BP over 24-48hrs to prevent hypoperfusion
  • rapid reduction in blood pressure, even to normal levels, may result in profound organ hypoperfusion as changes may have occured to mechanisms of BP control
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118
Q

tx options for hypertensive emergencies?

A
  • IV nitroprusside, labetalol, and GTN
  • phentolamine
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119
Q

phenotolamine?

A

(alpha-adrenergic antagonist) also used in phaeochromocytoma crisis.

120
Q

renal artery stenosis?

A
  • fibromuscular dysplasia of the renal artery is one of the most common causes of secondary hypertension and should be excluded by imaging(screening with duplex ultrasound, confirmation by angiography)
  • If fibromuscular dysplasia is detected, other vascular beds (i.e. cerebrovascular) should be screened
121
Q

what can HTN lead to?

A
  • TIA, stroke, dementia
  • heart failure, left ventricular hypertrophy
  • angina, myocardial infarct
  • peripheral vascular disease
  • fundal haemorrhages or exudate
  • renal impairment, proteinuria
122
Q

Assessing for end organ damage?

A
  • Test for haematuria.
  • Arrange measurement of:
  • Urinealbumin:creatinine ratio (to test for the presence of protein in the urine).
  • HbA1C (to test for diabetes).
  • Electrolytes, creatinine, and estimated glomerular filtration rate (to test for chronic kidney disease).
123
Q

other tests for end organ damage?

A
  • Examine the fundi (for the presence of hypertensive retinopathy).
  • 12 lead ECG(to assess cardiac function and detectleftventricular hypertrophy).
124
Q

screening for secondary causes of HTN

A
125
Q

Secondary causes of HTN that are screened for?

A
  • primary hyperaldosteronism/ Conns syndrome
  • phaechromocytoma
  • cushings syndrome
126
Q

Primary hyperaldosteronism/ Conn’s syndrome?

A
  • cause of up to 25% of drug resistant HTN
  • Aldosterone:renin ratio (ARR) is the first line test for the diagnosis of primary hyperaldosteronism
  • discontinuation of aldosterone antagonist (spironolactone and epleronone) and diuretics for 4 weeks prior to the test
127
Q

Phaeochromocytoma?

A
  • Rare cause
  • the diagnosis is more likely if the patient also has symptoms such as sweating, palpitations or frequent sweating.
  • check levels of plasma metanephrines
128
Q

cushings syndrome?

A
  • v rare cause
  • central weight gain
  • easy bruising
  • buffalo hump
  • round puffy face
  • proximal muscle weakness
  • abd striae
129
Q

cushings tests?

A
  • urine free cortisol - urine passed in 24 hours collected
  • late night salivary collection
  • overnight dexamethasone suppression test
130
Q

thyroid disease?

A
  • Hypo- and hyperthyroidism can both rarely cause secondary hypertension,
131
Q

symptoms of hypothyroidism:

A
  • tiredness
  • cold intolerance
  • weight gain
  • constipation
  • muscle weakness
132
Q

symptoms of hyperthyroidisim?

A
  • weight loss,
  • mood swings,
  • difficulty sleeping,
  • heat sensitivity,
    -palpitations
    -neck swelling
133
Q

lifestyle advice in HTN Mx?

A
  • lifestyle advice
  • ask about diet and exercise
  • discourage excessive consumption of coffee and other caffiene rich products
  • sodium intake low
  • inform patients of local incentives
  • advise ppl w hypertension who choose to self monitor BP to use HBPM
134
Q

BP target for those Under 80 with or without T2D, CKD, T1D with A:C ratio of less than 70?

A
  • below 140/90
135
Q

BP target for those with T1D plus A:C of >70mg/mmol or CKD plus A:C of >70?

A

below 130/80

136
Q

BP target for over 80s with or without diabetes?

A

150/90

137
Q

BP target for over 80s with CKD and an AC of under 70?

A

CKD plus A:C under 70
- below 140/90

CKD plus A:C of 70 or more
- below 130/80

138
Q

overall BP targets?

A
  • <80 reduce BP to under 140/90
  • > 80 reduce BP to below 150/90
139
Q

ACEi mechanism?

A
  • angiotensin 2 is a vasoconstrictor that causes aldosterone release
  • aldosterone causes renal sodium and fluid retention
  • downreg sympathetic adrenergic activitity by blocking the effects of A2 on sympathetic nerves
  • ACEi also increase bradykinin production which makes BVs dilate
140
Q

ACEi indications?

A
  • hypertension
  • HF
  • post MI
141
Q

side effects of ACEi?

A
  • dry cough
  • hypotension - especially in HF patients
  • hyperkalaemia - reduced aldosterone
142
Q

side effect of ACEi which is 2-4x higher in african americans?

A

angioedema

143
Q

when are ACEi contra-indicated?

A

pregnancy

144
Q

how do diuretics work?

A
  • inhibit sodium chloride transporter in DCT
  • increases potassium loss -> risk of hypokalemia
145
Q

when are aldosterone blocking diuretics used for HTN?

A
  • Potassium-sparing, aldosterone-blocking diuretics (e.g., spironolactone or eplerenone) are used in secondary hypertension caused by primary hyperaldosteronism
146
Q

Side effects of diuretics?

A
  • hypokalemia
  • metabolic alkalosis
  • dehydration (hypovolemia)
  • hyponatremia
  • hyperglycaemia in diabetics
147
Q

BBs mechanism in HTN?

A
  • decreased arterial BP by reducing CO
148
Q

side effects of BBs?

A
  • bradycardia
  • reduced exercise capacity
  • heart failure
  • hypotension
  • atrioventricular (AV) nodal conduction block.
  • from the excessive blockage of normal sympathetic influences
149
Q

what can BBs NOT be prescribed with?

A
  • can’t prescribe it with cardiac selective CCBs e.g. verpamil
150
Q

contra-indications of BBs?

A
  • CI with asthma due to bronchoconstriction
151
Q

how do CCBs work?

A
  • by causing vascular SM relaxation they decrease systemic vascular resistance which lowers arterial BP
  • some also reduce heart rate and contractility
152
Q

indications of CCBs?

A
  • hypertension
  • angina
  • arrhythmias
153
Q

cardio-selective nondihydropyridine CCBs?

A
  • verapamil and diltiazem
  • can cause excessive bradycardia, constipation, impaired electrical conduction (e.g., atrioventricular nodal block), and depressed cardiac contractility.
154
Q

CCBs espec non-dihydropyridines should not be administered to?

A
  • ppts w HF caused by systolic dysfunction
  • ppts on BBs as BBs also depress cardiac electrical activity
155
Q

Drug interactions: Beta blockers and verpamail and dilitiazem ->

A

bradycardia and AV block

156
Q

Verapamil and diliitizem with digoxin ->

A

digoxin toxicity mainly with verapamil

157
Q

Diuretics with digoxin ->

A

increased digoxin toxicity due to hypokalemia

158
Q

ACEi/ ARBs with diuretics ->

A

addiitive hypotensive action

159
Q

potassium sparing diuretics ->

A

hyperkalemia when used together

160
Q

compliance of anti-hypertensive meds?

A
  • poor compliance
  • reminders/ phone apps to measure BP
  • promote self care and education
  • awareness of risks
161
Q

metabolic syndrome?

A

hypertension, diabetes, obesity and hypercholesterolemia

162
Q

Sx of MS

A
  • large weight circumference
  • symptoms of diabetes - inc thirst and urination
  • fatigue
  • blurred vision
163
Q
A
164
Q

Causes of MS?

A
  • overweight/ obesity
  • insulin resistance syndrome
165
Q

RF for metabolic syndrome?

A
  • FHx
  • poor diet
  • inadequate exercise
166
Q

pathophys of MS?

A
  • insulin resistance
  • pancreatic beta cell dysfunction
  • Chronic inflammation
  • Suppression of insulin receptor substrate-1 and 2 (IRS1/IRS2) gene expression and function
167
Q

what is primary prevention?

A
  • population strategy
  • targeted strategy
168
Q

population strategy?

A

modifying RF for whole population through diet and lifestyle advice on basis that a small reduction in smoking, cholesterole etc will produce worthwhile benefits

169
Q

targeted strategy?

A
  • identify high risk individuals using scoring systems and treat RF by medication
170
Q

secondary prevention?

A
  • people who alr have evidence of athermatous vascular disease and @ high risk of futyre CV events
  • should all be given a statin and BP target 140/85
171
Q

groups that CVD risk tools might underestimate risk for:

A
  • people treated for HIV
  • people who have recently stopped smoking
  • people who are already taking meds to treat CVD
  • ppl w severe mental illness
172
Q

choice of anti-hypertensive

A
  • add spironolactone 4th line if K <4,5
  • add alpha blocker otherwise
173
Q

CVD risk - explore the person’s?

A

beliefs about what determines future health (this may affect their attitude to changing risk)

174
Q

CVD risk - assess?

A
  • assess their readiness to make changes to their lifestyle (diet, physical activity, smoking and alcohol consumption), to undergo investigations and to take long-term medication
  • assess their confidence to make changes to their lifestyle, undergo investigations and take medication
175
Q

CVD risk - inform them of?

A

potential future management options based on current evidence and best practice

176
Q

asthma =

A
  • chronic - lM lung condition leading to variable and recurring symptoms
  • characterised by intermittent obst and hyperresponsiveness of the airways - affects large and small airways
    causes
177
Q

what causes asthma?

A
  • meds: beta blockers
178
Q

triggers for asthma?

A
  • grass
  • pollen
  • house dust mites
  • pets
179
Q

what happens in asthma?

A
  • T2h cell driven
  • IgE: early onset asthma, allergic asthma
  • eospinophilic asthma tends to occur in middle aged patients - IL 4, IL5, IL13
180
Q

who does neutrophilic asthma tend to affect?

A

female, smoker, obese patietns

181
Q

usual asthma symptoms?

A
  • intermittent dry cough sometimes productive
  • intermittent wheezing nocturnal symptoms
  • SOB
182
Q

Bedside measurement for asthma?

A
  • peak flow
  • asthmatics will show variation - morning will be low and will be better during the day
183
Q

Other tests for asthma in adults

A
  • CXR rules out pneumonia and PE
  • FeNO- shows if there’s eosnophilic inflammation
184
Q

when there is both COPD and asthma =

A

overlap syndrome

185
Q

management of acute asthma in adults - assessment of severity

A
186
Q

near fatal asthma =

A

when CO2 becomes raised

187
Q

management of asthma

A

oxygen
1) steroids
2) beta agonists and AM for bronchodilation
3) magnesium sulfate injected
4) ipatropium

188
Q

acute asthma in pregnancy?

A
  • give drug therapy as for the non pregnant patient
  • continuous fetal monitoring recommended for severe acute asthma
189
Q

why predict CV risk?

A
  • to allow weighing up costs and benefits of treatment
190
Q

Number needed to treat =

A
  • is the number of patients you need to treat to prevent one additional bad outcome (death, stroke, etc.).
  • For example, if a drug has an NNT of 5, it means you have to treat 5 people with the drug to prevent one additional bad outcome.
191
Q

population attributable risk?

A
  • population attributable risk: represents the proportion of all the disease risk in a population that may be caused by a factor.
  • it illustrates how much of the risk in the population would be removed if that risk factor was not present (or was successfully treated).
192
Q

CVD risk prediction charts?

A
  • joint british socities 10 year CVD risk prediction charts
  • underestimates when there’s impaired glucose regulation and when the ppt is * Indian, Pakistani, Bangladesh or Sri Lankan
193
Q

focusing interventions based on the risk level of the patient means?

A
  • By focusing interventions on those at highest risk we focusing the possible benefits on those with most at stake.
  • Some interventions such as drugs carry harms of their own. By focusing their use on individuals at high risk of disease we ensure that the risk of harm:benefit remains low.
194
Q

Other methods of risk prediction?

A
  • SCORE
  • ASSIGN - takes into acount SES
  • QRISK - derived from the experience of UK patients identified and followed in GP record systems
195
Q

% of HTN cases caused by secondary HTN?

A
  • 95% of HTN cases caused by essential HTN
  • 5-10% of cases caused by secondary HTN
196
Q

BBs in the Tx of HTN?

A
  • added late in the Tx of HTN
  • consider them for younger people especially women of childbearing age or people with intolerance/ CI to ACEi/ARBs
197
Q

When should ACEi not be used?

A
  • renovascular disease
198
Q

alpha blockers indications?

A
  • benign prostatic hypertrophy/ HTN
199
Q

contra-indications of alpha blockers?

A

urinary incontienence

200
Q

signs of aortic coarctation?

A

radio-femoral delay or weak femoral pulses

201
Q

benefits of smoking cessation?

A
  • smokers who quit at 25 to 34 years had survival curves nearly identical to those who never smoked, with a ten-year survival gain compared to current smoker
  • lowered risk of stroke, TIA, cardiovascular diseases, lung cancer
  • improved mortality
202
Q

smoking cessation: lower risk of?

A
  • less cancer risk: liver, stomach, pancreatic, kidney, cervix etc - linked to over 12 types of cancer
203
Q

Primary prevention of CV disease?

A
  • aims to keep an individual at risk of cardiac events from having them
  • usually aimed at people who have aleady developed CV risk factors such as hypertension
  • focuses on controlling RF by making healthy lifestyle changes e.g.
  • statins if lifestyle change is ineffective/ inappropriate
204
Q

Secondary prevention of CV disease?

A
  • after someone has a cardiac event or undergoes angioplasty or bypass surgery, or develops some other form of heart disease
  • medications like aspirin/ statins
  • smoking cessation and weight loss
205
Q

what is the point of secondary prevention of CV disease?

A
  • prevention of further cardiac events, halts progression of heart disease, prevention of early death
  • start statin treatment and consider lifestyle changes
206
Q

Preventative measures?

A
  • behaviour changes
  • healthy eating - eat well guide
  • cardiprotective diet - reducing saturated fats and salt intake
  • physical activity - aerobic and muscle strengthening activities
  • weight management
  • reducing alcohol consumption and smoking cessation
207
Q

Aspirn?

A
  • irreversibly inhibits COX-1 and COX-2
  • Inhibition of COX-1 results in the inhibition of platelet aggregation for 7-10 days
  • inhibition of COX-1 also reduces production of prostaglandins which stops the conversion of arachidonic acid to thromboxane A2 which is a platelet aggregator
208
Q

statins mechanism?

A
  • inhibition of HMG-CoA reductase
209
Q

ezetimibe?

A
  • inhibitor of cholesterol absorption
  • targets NPC1L1 protein which is expressed on eneterocytes
210
Q

Epidemiology of CV disease?

A
  • In developed countries heart disease and stroke are the first and second leading cause of death among adult men and women.
  • Twice as many deaths from CVD occur in developing countries as in developed countries
  • main cause of death in the UK
211
Q

Outline a strategy to reduce cardiovascular disease in the local community?

A
  • Encouraging smoking cessation
  • education on the impacta of smoking and beenfits of smoking cessation
  • NHS Smokefree website and referral to smoking cessation clinics
212
Q

arryhthmia =

A

abnormal heart rate or rhythm

213
Q

Symptoms of arrythmias?

A
  • asymptomatic
  • palpitations
  • decompensated failure
  • syncope
  • sudden death
214
Q

types of arrythmias?

A

brady-arrythmias and tachy-arrythmias

215
Q

bradyarrythmias?

A

sinus arrythmia or sinus arrest, or AV block

216
Q

SA/ sinus arrest?

A

sinus pauses or sick sinus syndrome - episodes of brady and tachy A - e.g. AF

217
Q

first degree AV block?

A
  • conduction within the AV node is slowed
  • benign condition, doesn’t require Tx
218
Q

what are the types of second degree HB?

A
  • Mobitz type 1: sometimes requires pacemaker
  • Mobitz type 2: always requires a pacemaker
219
Q

Third degree AV block?

A
  • always requires a pacemaker
  • complete HB - no signal transmitted through AVN
220
Q

A patient who is in permanent AF who has a rhythm that suddenly becomes regular/ slow =

A

equiv to complete hB

221
Q

tachy-arrhythmia can be classified depending on whether they’re ?

A
  • narrow complex
  • broad complex
222
Q

narrow complex ARS means

A

< 120ms

223
Q

a narrow complex QRS and irregular rhythm is usually

A

AF

224
Q

Narrow QRS + regular R?

A

sinus tachycardia, atrial flutter, AVRT/ AVNRT

225
Q

Broad complex tachycardia with a regular rhythm can be:

A
  • ventricular tachycardia - it’s this unless ECG shows otherwise
  • SVT + BBB
  • sinus tachy + BBB
226
Q

broad complex tachycardia with irregular rhythm?

A
  • EXCLUDE V FIB
  • could be A fib w BBB
227
Q

what to look for on an ECG for arrythmias?

A
  • rate
  • rhythm - regular, irregular, irregularly irregular - broad/ narrow complexes
228
Q

first degree AV block?

A
  • Conduction slowed at the AVN
  • gives a prolonged PR interval
  • > 200ms PR interval
229
Q

second degree AV block - type 1/ wenchebach?

A
  • P-R interval progressively prolongs each beat then beat (QRS) drops
    -type 2: normal PR then beat drops
230
Q

what can second degree AV block be due to?

A

BBs or a high vagal tone

231
Q

Type 2, 2:1 AV block?

A
  • every second beat goes through the AV node
  • usually due to structural AV node disease
232
Q

How serious is 2:1 AV block?

A
  • always progresses to complete heart block, requires a pacemaker
233
Q

Second degree AV block Type 1 ECG

A
234
Q

How does 2:1 AV block look

A

P QRS P then P QRS

235
Q

2nd degree 3:1 AV block?

A
  • 3 P waves for every QRS
236
Q

3rd degree AV block (complete heart block)

A
  • complete blockage at the AV node so no impulses get through from the SAN - no P waves conducted through
  • ventricles start pacing themselves but ventricular pacemaker cells are at a lower rate so usually slow
  • much more unstable pathway -> if untreated usually leads to death within 6 weeks
237
Q

how serious is complete heart block?

A
  • much more unstable pathway -> if untreated usually leads to death within 6 weeks
238
Q

when is an immediate ppm required for 3rd degree AV block?

A
  • immediate ppm if syncope or HR <35bpm
239
Q

Complete HB ECG?

A
  • can see P waves and QRS on ECG but no consistent pattern to them
  • P waves at regular intervals
240
Q

LBBB?

A
  • Signal travels down the right branch
  • has to move over the left from the right branch in order for the left bundle to depolarise
  • depolarisation takes longer so broad QRS
241
Q

LBBB ECG?

A
242
Q

RBB?

A
  • SAN -> AV -> LBBB then moves across to RBB slowly
  • broad QRS
243
Q

RBBB ECG?

A
  • RSR in V1 and V2/ V3
  • wide S wave in lateral leads
244
Q

What are the narrow complex (regular) tachycarrythmias?

A
  • sinus tachy
  • atrial flutter
  • AVRT/ AVNRT
245
Q

Atrial flutter?

A
  • regular re-enterance circuit going around RA
  • normal QRS
246
Q

AV node re-entrant tachycardia?

A
  • repeating loop at the AV node which passes on a rapid rate to ventricles
  • no P waves bc its not the SAN thats activating
  • narrow normal QRS complexes
  • same ECG as AVRT
247
Q

AVNRT ECG

A
248
Q

AV re-rentrant tachycardia?

A
  • additional conductive pathway occurs elsewhere between the atria and ventricle
  • e.g. wolf parkinson white syndrome
249
Q

AVRT ECG?

A
  • impulses being trabsmitted through to the ventricles at a fast rate
  • no P waves
  • narrow complex unless additional block
  • regular
  • might get delta waves which make the QRS complex more broad
250
Q

Narrow complex irregular tachycardia?

A

AF

251
Q

What happens in AF?

A
  • chaotic activity within atria
  • intermittently randomly passes through AVN
  • narrow complex QRS
252
Q

ECG of AF?

A
  • no P waves
  • narrow complex
  • irregular tachycardia
253
Q

Broad complex regular tachycardias?

A
  • ventricular tachycardia
  • ventricular fibrillation
254
Q

what happens in ventricular tachycardia?

A
  • abn tissue within ventricle (often related to scar after a heart attack) can form a re-enterant loop that runs around the ventricle
  • abn conduction within ventricle means QRS is broad and re-enterant loop is rapid so fast re-enterant tachy
255
Q

Ventricular tachycardia ECG?

A
  • no P waves
  • broad complex of single morphology
256
Q

V fib ECG?

A
  • no P waves
  • broad complex irregular tachycardia - looks like a child’s scribbles
257
Q

assessment of arrythmias - ABCDE?

A
  • monitor O2 and give oxygen if hypoxic
  • ECG, BP and 12 lead ECG
  • obtain IV access
  • identify and treat reversible causes i.e. electrolytes paticularly potassium
258
Q

Adverse features of arrythmias?

A
  • shock
  • syncope
  • if yes and the patient has a tachyarrythmia we need to cardiovert the patient, 3 attempts of this
  • if this doesn’t work try chemical cardioversion with amiodarone, repeat shock, give more amiodarone
259
Q

Tx of AVNRT or flutter?

A
  • vagal manouvers
  • adenosine
  • continous ECG monitoring
260
Q

adenosine?

A
  • adenosine blocks AV node which will stop an AVNRT or pause activity through AV node allowing flutter waves to be seen
  • continous monitoring through this
261
Q

Atrial fibrillation Tx?

A
  • rate control - BBs, digoxin, amiodarone
  • anticoag
  • consider DCCV if no thromboembolic risk
262
Q

Broad QRS - reg vs irregular rhythm?

A
  • irregular rhytm -> seek expert help
  • rule out V fib
  • reg R - rule out ventricular tachycardia (serious arrythmia)
  • both may need immediate cardioversion
263
Q

Broad QRS

A
264
Q

breathlessness from pulm oedema?

A

Shortness of breath can manifest as orthopnea (inability to lie down flat due to breathlessness) and/or paroxysmal nocturnal dyspnea (episodes of severe sudden breathlessness at night)

265
Q

PO chest XR findings?

A
  • Chest X-ray will show fluid in the alveolar walls,
  • Kerley B lines, increased vascular shadowing in a classical batwing peri-hilum pattern,
  • upper lobe diversion (increased blood flow to the superior parts of the lung), and possibly pleural effusions.
266
Q

IPF most common clinical features?

A
  • age over 50 years,
  • exertional dyspnea,
  • inspiratory bibasilar “velcro-like” crackles on auscultation, clubbing of the digits,
  • abnormal pulmonary function test results, with evidence of restriction (low FVC with normal FEV1/FVC ratio)
267
Q

drug which causes dry mouth and urinary retention?

A
  • tiotropium
  • anticholingeric effects of muscarnic antagonist
268
Q

What is the most common mode of presentation of mesothelioma?

A

Breathlessness from pleural effusion

269
Q

feature of LVF?

A

A left ventricular 3rd heart sound

270
Q

Treatable causes of HTN?

A
  • Hypokalaemia
  • Disease states that lead to abnormally high aldosterone levels can cause hypertension and excessive urinary losses of potassium.
  • These include renal artery stenosis and tumors (generally non-malignant) of the adrenal glands, e.g., Conn’s syndrome
  • Cushings synfrome
271
Q

analine dyes may cause?

A

lung cancer

272
Q

coal mining leads to?

A

fibrosis

273
Q

occupations most linked to asthma?

A
  • spray painting
  • food processing
  • nurses
  • chemical workers
  • those who work with animals
  • welders
  • hairdressers
  • timber workers
274
Q

Production of what

role of eosinophils in asthma?

A

leukotriene production

275
Q

characteristid pathophys of an acute asthma exacerbation?

A

bronchial mucus plugging

276
Q

high protein and LDH pleural effusion cause?

A

The high protein and LDH suggest an exudate, commonly secondary to malignancy or infection

277
Q

doasge of LMWH?

A

based on body weight

278
Q

pleuritic chest pain?

A
  • originates from parietal pleura (VP has no sensory innervation)
  • associated with a frction rub
279
Q

drug which does not interact w warfarin?

A

furosemide

280
Q

warfarin and alcohol?

A

Excessive use of alcohol is also known to affect the metabolism of warfarin and can elevate the INR

281
Q

IPAH?

A
  • Is associated with chest pain, dyspnoea and syncope, ESPEC in adolescence
  • Is secondary to inc foetal pulm HTN
  • more common in females
282
Q

Pulmonary Hypertension is most severe in which untreated valvular disease?

A
  • mitral stenosis
283
Q

signs and symptoms of IE?

A

FROM JANE

  • Fever
  • Roth’s spots
  • Osler’s nodes
  • Murmur
  • Janeway lesions
  • Anemia
  • Nail hemorrhage (splinter hemorrhages)
  • Emboli
284
Q

what does not cause pleural effusion?

A

IPF

285
Q

Amiodarone toxicity?

A
  • interstitial pneumonitis secondary to amiodarone causing fibrosis and a restrictive pattern on pulmonary function testing
  • One characteristic finding in all patients exposed to amiodarone is the presence of numerous foamy macrophages in the air spaces.
286
Q

Which oral rate limiting medication will produce the quickest effect in AF?

A

Metoprolol - rapid onset

287
Q

ankle swelling from amlodepine mechanism?

A
  • The peripheral oedema associated with calcium channel blockers is related to redistribution of fluid from the vascular space into the interstitium.
  • `increased calcium channel blocker-mediated vasodilation leads to increased pressure and subsequent permeability in the capillary circulation.
288
Q

which drugs when combined risk hyperkalaemia?

A
  • multiple inhibitors of the RAAS system
  • ACE inhibitors, angiotensin receptor blockers and aldosterone antagonists all cause a rise in serum potassium which can be additive when combined
289
Q

clarithromycin strongly interacts with?

A

statins

290
Q

Angina Ix?

A

For patients in whom stable angina cannot be excluded by clinical assessment alone NICE recommend the following (e.g. symptoms consistent with typical/atypical angina OR ECG changes):

1st line: CT coronary angiography
2nd line: Non-invasive functional imaging (looking for reversible myocardial ischaemia)
3rd line: Invasive coronary angiography

291
Q

Examples of non-invasive functional imaging:

A
  • Myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT) or
  • Stress echocardiography or
  • First-pass contrast-enhanced magnetic resonance (MR) perfusion or
    MR imaging for stress-induced wall motion abnormalities
292
Q

muscle weakness, tetatany, cramps or arrythmias ->

A

primary hyperaldostosteronism

293
Q

rapid onset acute PO ->

A

renal artery stenosis

294
Q

sweating, palpitations, freq headaches ->

A

phaechromocytoma

295
Q

snoring or daytime sleepiness ->

A

OSA

Year 3 (45 decks)

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