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Phase 2a NEW > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Atherosclerosis

A

Plaque rupture
Thrombus formation
Partial/complete arterial blockage
Heart attack, stroke or gangrene

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2
Q

RFs for atherosclerosis

A 
Increasing age
Smoking
Raised cholesterol
Obesity 
Diabetes
Hptn
Fx
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3
Q

Distribution of atherosclerotic plaques

A

Peripheral and coronary arteries
Focal distribution along artery length
Distribution governed by haemodynamic factors - Changes in blood flow/turbulence (such as bifurcations) cause the artery to alter endothelial cell function

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4
Q

Structure of an atherosclerotic plaque

A

Lipid
Necrotic core
Connective tissue
Fibrous cap

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5
Q

Plaque

A

Occlusion - Angina

Rupture - Thrombus formation (and death)

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6
Q

Causes of inflammation in arterial wall

A

LDL - Accumulates in arterial wall

Endothelial dysfunction due to injury

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7
Q

Stimulus for adhesion of leukocytes

A

Once inflammation is initiated, chemoattractants (chemicals that attract leukocytes) are released from endothelium and send signals to leukocytes
Chemoattractants are released from site of injury and a conc grad is produced
Stimulus = Chemoattractants

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8
Q

Inflammatory cytokines found in plaques

A

IL-1,6,8
IFN Gamma
CRP

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9
Q

Leukocyte recruitment to vessel walls

A

Mediated by selectins, integrins and chemoattractants

Cause leukocytes to roll, adhere and transmigrate

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10
Q

Progression of atherosclerosis - Stage 1

A

Fatty streaks - earliest lesion of AS

Early ages - less than 10 y.o

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11
Q

Progression of atherosclerosis - Stage 2

A

Intermediate lesions
Composed of foam cells (lipid laden macrophages), vascular smooth muscle cells, T lymphocytes, adhesion and aggregation of platelets to vessel wall, isolated pools of extracellular lipid

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12
Q

Progression of atherosclerosis - Stage 3

A

Advanced lesion - Fibrous plaque
Impedes blood flow
Prone to rupture
Dense fibrous cap made of collagen (strength) and elastin (flexibility) laid down by smooth muscle cells
May be calcified
Contains smooth muscle cells, macrophages, foam cells and T lymphocytes

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13
Q

Progression of atherosclerosis - Stage 4

A

Plaque rupture
Plaque is constantly growing and receding (resorbed and redeposited)
Cap becomes weak and plaque ruptures
Thrombus formation and vessel occlusion

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14
Q

Progression of atherosclerosis - Stage 5

A

Plaque erosion
Lesions tend to be early lesions
Fibrous cap thick may

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15
Q

Treating coronary artery disease

A

PCI - Percutaneous coronary intervention

Stent implantation

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16
Q

Restenosis

A

Narrowing/blocking of vessel lumen after surgical correction

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17
Q

Drug elution

A

Anti-proliferative and inhibits healing

Reduce restenosis

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18
Q

Useful drugs in atherosclerosis

A

Aspirin
Clopidogrel
Statins

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19
Q

ECG and drug toxicity

A

Digoxin prolong the QT interval

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20
Q

Depolarisation

A

Contraction of a muscle

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21
Q

Pacemakers of the heart

A

SAN (Dominant) - 60-100bpm
AVN (Back-up) - 40-60bpm
Ventricular cells (Back-up) - 20-45bpm

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22
Q

Standard calibration of an ECG

A

25mm/s (speed)

0.1mV/mm (voltage)

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23
Q

Impulse conduction

A 
SAN
AVN
Bundle of his
Bundle branches
Purkinje fibres
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24
Q

PQRST

A

P - Atrial depolarisation
QRS - Ventricular depolarisation
T - Ventricular repolarisation
PR interval - allows time for atria to contract before ventricles

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25
Q

1st degree heart block

A

Long PR interval

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26
Q

QRS abnormalities

A

Ventricular enlargement

Conduction blocks

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27
Q

Angina types

A

Prinzmetal’s angina (coronary spasm)
Microvascular angina
Crescendo angina
Unstable angina (Critical ischaemia - plaques severely occluding artery)

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28
Q

IHD history

A 
Personal details
Presenting complaint 
Past med history
Drug history, allergies 
Fx (only first degree relatives)
Social history (smoking)
Systematic enquiry
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29
Q

Cardiac symptoms

A 
Chest pain
Breathlessness
Fluid retention (HF)
Palpitation 
Syncope or pre-syncope
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30
Q

Pain

A 
OPQRST
Onset
Position (site)
Quality (nature/character)
Relationship (exertion, posture, meals, breathing, etc)
Radiation (Throat, arm, upper body)
Relieving/aggravating factors 
Severity 
Timing
Treatment (does it work immediately)
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31
Q

Chest pain - Differential diagnosis

A 
MI
Pericarditis/myocarditis 
Pulmonary embolism/pleurisy 
Chest infection/pleurisy 
Dissection of aorta 
Gastro-oesophageal (reflux, ulceration, spasm)
MSK - Arthritis 
Psychological - Anxiety
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32
Q

Treatment

A

Lifestyle - Smoking, weight, exercise, diet
Advice for an emergency - 999
Medication
Revascularisation

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33
Q

NICE guidelines for angina - GP

A

History - typical/atypical angina?
Exam - exacerbating causes
Investigations - Routine bloods, lipids, ECG
Angina? - Refer to cardio
Treat - Smoking cessation, aspirin, BB, statin, GTN spray

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34
Q

NICE guidelines for angina - Cardiologist

A

Diagnostic test - CTCA (CT coronary angiogram)

High risk/CTCA shows stenoses - Refer to cath lab

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35
Q

Exercise testing

A

The patient runs on treadmill whilst ECG records

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36
Q

Myoview scan

A

Perfusion scan

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37
Q

Stress echo

A

Echocardiogram

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38
Q

Perfusion MRI scan

A

Gold standard

Indicates the structure and function of the heart - any ischaemic areas are highlighted

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39
Q

Invasive coronary angiography

A

Through radial artery

Not diagnostic, more about treatment planning (what interventions are appropriate)

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40
Q

Angina - 1st line drug - BB

A

BB - Lowers HR, Lowers LV contractility which together lower cardiac output and demand
SEs of BB - Tiredness, bradycardia, cold hands and feet, erectile dysfunction
CIs of BB - Asthma patients

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41
Q

Angina - 2nd line drug - Nitrates

A

Dilate vessels and reduce preload on the heart
Dilate coronary vessels
SE - Headache

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42
Q

Angina - 3rd line drug - CCB

A

Reduce afterload on the heart
Dilate arterial vessels
SE - Flushing, swollen ankles, postural hypotension

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43
Q

Angina - 4th line drug - Aspirin

A

Antiplatelet and anti-inflammatory
Cyclo-oxygenase inhibitor
SE - Gastric

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44
Q

Angina - 5th line drug - Statins

A

HMG CoA reductase inhibitors

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45
Q

Angina - 6th line drug - ACEi

A

Ramipril

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46
Q

Revascularisation

A

PCI/CABG

MDT meeting

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47
Q

Coronary angioplasty/Stenting -

A

PCI - Percutaneous coronary intervention

Risks - stent thrombosis, restenosis

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48
Q

CABG

A

If a stent is not appropriate then bypass is next step
Coronary artery bypass graft
Risks - v invasive, stroke risk, chest bleeding risk

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49
Q

PCI and CABG use

A

STEMI - PCI
NSTEMI - PCI>CABG
Stable angina - PCI/CABG

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50
Q

Unstable angina

A

Cardiac chest pain at rest

Diagnosis - Troponin level is not increased

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51
Q

Acute MI

A

ST elevation

Non ST elevation - retrospective diagnosis

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52
Q

MI - ECG features

A

ST elevation - can be inverse which confirm MI
Q waves - broad and deep indicate pathology
Poor R wave progression
Biphasic T wave

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53
Q

MI

A

Cardiac chest pain - persistent, severe but can be mild, occurs at rest, sweating, breathlessness, N/V
Causes permanent heart muscle damage
Higher risk - higher age, diabetes, renal failure, left ventricular systolic dysfunction

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54
Q

MI - Initial management

A

999
If ST elevated - transfer to PCI
Aspirin immediately
Pain relief

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55
Q

MI - hospital management

A

Oxygen therapy - if hypoxic
Pain relief - Narcotics/nitrates
Antiplatelets - Aspirin +/- P2Y12 inhibitor
BB
Coronary angiography - If troponin elevated

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56
Q

MI - Causes

A

Atherogenesis/atherothrombosis

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57
Q

Troponin

A

Protein complex regulates actin/myosin contraction
Highly sensitive marker for cardiac muscle injury
Not specific for ACS

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58
Q

Antiplatelet drugs

A

Aspirin

Streptokinase

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59
Q

P2Y12 inhibitors

A

Clopidogrel
Used in combo with aspirin to manage ACS (Dual antiplatelet therapy)
Clopidogrel is a prodrug - activated by CYP450 enzymes
Drug interactions - Omeprazole
Tricagelor (rapid onset and offset) is preferred over clopidogrel (much more irreversibly bound to CYP450 which makes offset delayed)
Adverse effects - Bleeding (GI), haematuria, rash

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60
Q

Anticoagulants

A

Target thrombin
Inhibit fibrin formation and platelet activation
Heparin used during PCI/CABG

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61
Q

ACS - Order of medication

A 
Initial pain relief - Morphine/nitrates
Antiplatelet - Aspirin + clopidogrel
Anticoag - Heparin
BB, CCB
Statins, ACEi
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62
Q

Heart weight

A

Heavier in males than females

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63
Q

Heart is composed of these proteins

A

Sarcomere proteins

Protein conformational change = contraction

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64
Q

Heart contraction

A

2 stage electrical generated contraction

Contractioon initiated by depolarisation and changes to calcium conc

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65
Q

Heart relaxation

A

Removal of calcium mediates relaxation

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66
Q

Types of cardiac myocytes

A

AV conduction system (fast conduction)

General cardiac myocyte

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67
Q

Heart failure

A

Failure to transport blood out of heart

Cardiogenic shock - severe failure

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68
Q

Myocardial hypertrophy

A

Athletes

Pregnancy

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69
Q

Diabetic complications

A 
Stroke 
CVD (leading cause of mortality)
Peripheral vascular disease
Diabetic retinopathy, Blindness
Diabetic neuropathy
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70
Q

Diabetic neuropathy - Consequences

A

Pain - burning, paraesthesia, nocturnal exacerbation, sharp and shoots up legs
Autonomic - Diarrhoea, urinary incontinence, erectile dysfunction
Insensitivity - Foot ulceration, infection, falls (lead to amputation)

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71
Q

Diabetic peripheral neuropathy

A

Typical ‘glove and stocking’ sensory loss

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72
Q

DN - Risk factors

A

Hptn
Smoking
Hba1c

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73
Q

DN - Treatment

A

Glycaemic control
SSRIs
Anticonvulsants - Carbamezapine, gabapentin)
Opioids - Tramadol, oxycodone

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74
Q

Diabetic foot ulceration

A

15% of people with DM

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75
Q

Diabetic amputation - pathophysiology

A 
Neuropathy or vascular cause
Trauma
Ulcer
Failure to heal
Infection 
Amputation
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76
Q

Neuropathy

A

Painless nature of diabetic foot disease

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77
Q

DN - Complications

A

Motor nerve damage
Localised callus (hard skin)
Autonomic nerve damage - dry skin which leads to cracks/fissures and makes feet susceptible to infection. Treat by moisturising twice a day

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78
Q

DPN - Screening tests

A

Test sensation - Monofilament, neurotip, tuning fork

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79
Q

Peripheral vascular disease

A

Decreased perfusion due to macrovascaular disease
More distal sites
Ischaemia in legs
High rates of amputation

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80
Q

PVD - Symptoms

A

Intermittent claudication - pain and cramping (ischaemic legs)

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81
Q

PVD - Signs

A

Absent pedal pulses
Coolness of deet
Poor skin and nails

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82
Q

PVD - Investigation

A

Doppler

Duplex arterial imaging

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83
Q

PVD - Treatment

A

Smoking cessation
Surgery
MDT foot clinic (for ulcers)
Pressure-relieving footwear, podiatry

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84
Q

Diabetic retinopathy

A

The commonest cause of blindness in adults

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85
Q

DR - RFs

A

Diabetes (chronic)
Poor glycaemic control - Hba1c raised
Hptn
Pregnancy

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86
Q

DR - Eye screening

A

Retinal photographs

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87
Q

DR - Pathogenesis

A

Leakage of blood vessels
Occlusion of blood vessels
Micro-aneurysms - Pericyte loss and smooth muscle cell loss
Basement membrane thickens
Reduces junctional contact with endothelial cells
Glial cells grow down capillaries - Ischaemia and occlusion due to proliferation
These lead to changes in the retina and then blindness occurs as a result

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88
Q

DR - Treatment

A

Laser therapy - burns off abnormal blood vessels to prevent leakage etc
Not curative, just stabilises disease to prevent progression to blindness
Photocoagulation - burns as much of retina as possible, which unfortunately leads to tunnel vision with only central vision surviving

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89
Q

Diabetic nephropathy

A

Diabetes is main cause of end stage renal disease

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90
Q

Diabetic nephropathy

A

Hallmark is proteinuria
Progressive decline in renal function
RFs - Poor BP and BG control
Major RF for CVD

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91
Q

Diabetic nephropathy - Pathogenesis

A

Glomerulus changes - Thickening of BM
Glomerular injury
Filtration of proteins
DN occurs

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92
Q

End-stage renal disease

A

Stage 5 CKD

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93
Q

Nephropathy in T1DM and T2DM

A

T1DM - Microalbuminuria develops 5-10 years after diagnosis

T2DM - Microalbuminuria present at time of diagnosis

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94
Q

Diabetic nephropathy - Treatment

A

ACEi

Statins - Cholesterol control

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95
Q

Diabetes screening

A

Urine dip - Albumin:Creatinine ratio
Retinal photography
Foot exam (10g monofilament)

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96
Q

T2DM meds - Insulin sensitisers (first line)

A

Metformin

Pioglitazone

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97
Q

T2DM meds - Increase beta-cell function (second line)

A

Sulphonylureas
DDP4i
GLP1 receptor agonists

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98
Q

Diabetes lab tests

A 
Fasting plasmaa glucose 
Hba1c
Na, K, Ur, Crt
Urine - Alb:Crt ratio
LFTs - AST, ALT
Lipids - T Chol, HDL, Trig
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99
Q

Diabetes - Lifestyle interventions

A

Local education programmes - In sheffield = Desmond and xpert
Exercise - 30mins a day
Dietician

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100
Q

T2DM - Pharmacotherapy regimen

A

1st line - Metformin (reduces insulin resistance) - Weight neutral/loss
2nd line - Sulphonylurea - Weight gain occurs
3rd line - DPP4i - Prolongs action of GLP1 (no weight change with DPP4i). GLP1 induce weight loss
4th line - SGLT2i (Reduce reabsorption of glucose in kidneys in proximal tubules from going back into the bloodstream) - Weight loss
5th line - Insulin - Weight gain

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101
Q

Bariatric surgery

A

Surgical weight loss in T2DM
BMI above 35
Reduce stomach size (gastric bypass) so patients appetite is reduced and weight loss occurs
Improves glycaemic control

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102
Q

DVT - Symptoms

A

Pain

Swelling

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103
Q

DVT - Signs

A

Tenderness
Swelling
Warmth
Discolouration

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104
Q

Proximal DVT

A

More problematic

Between hip and knee

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105
Q

DVT - Investigations

A

Ultrasound compression test for proximal veins (popliteal fossa) - if vein squashes flat then no DVT, if can’t squash flat then DVT possible
D-dimer blood test - Normal result excludes diagnosis, Raised result is not specific for thrombosis (cannot confirm diagnosis)
D-dimer is used after ultrasound to confirm diagnosis
Infection and inflmmation can raise D-dimer level which is why it’s not specific for DVT
Raised D-dimer is common

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106
Q

Low Hb =

A

Anaemia

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107
Q

DVT - Treatment

A

1st line - LMW Heparin (anticoag) - minimum 5 days
2nd line - Oral Warfarin (anticoag) - 3-6 months
DOAC - Direct-acting oral coag
Compression stockings - Decrease swelling and risk of long term post-thrombotic syndrome

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108
Q

DVT - Causes

A

Thrombophilia

Malignancy

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109
Q

DVT - RFs

A 
Surgery
Immbolity 
Leg fracture 
Pregnancy (Oestrogen raised)
Long haul flights/travel (rare though)
Inherited thrombophilia (genetic predisposition) - Caucasians
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110
Q

DVT - Prevention

A 
Compression stockings
Early mobilisation 
Hydration 
Mechanical foot pumps
Chemical thromboprophylaxis - LMW Heparin
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111
Q

Thromboprophylaxis

A

Not required in young patients having short duration surgery

Required in high risk, long duration surgery

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112
Q

Pulmonary embolism

A

DVT which has broken off from vein and gone through heart and blocking up pulmonary artery
A big clot will block up both./bifurcation of pulmonary aeries and results in death

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113
Q

Pulmonary embolism

A

Hypotension
Cyanosis
Severe dyspnoea
Right heart failure

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114
Q

Pulmonary embolism - Removal

A

Embolectomy

Thrombolysis - mechanical or chemical (tPA)

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115
Q

Pulmonary embolism - Presentation

A 
Chest pain - pleuritic 
SOB/breathlessness
Haemoptysis - if pulmonary infarct
Signs of DVT in legs
Signs - Tachycardia, tachypnoea
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116
Q

PE - Investigations

A

CXR - Usually normal
ECG - May show sinus tachycardia, ECG to rule out cardiac causes
D-dimer - raised then do imaging, if normal then no pulmonary embolus (not specific though)
CTPA - Spiral CT with contrast, visualise major segmental thrombi - major diagnostic tool
Ventilation/perfusion scan - Mismatch defects

117
Q

PE - Treatment

A

Same as DVT - LMW Heparin then warfarin/Or DOAC (Only in outpatients with minor PE)
If cannot anti-coag, consider IVC filter insertion to prevent further PE, however, legs may embolise as a result

118
Q

PE - Prevention

A

Same as DVT

119
Q

Warfarin

A 
Oral
Works on liver
Prevents synthesis of active factors - 2,7,9,10 (still synthesised but do not work, does this by interfering with VitK pathway)
VitK antagonist
Long half-life
Prolongs prothrombin time 
Narrow therapeutic range - have to keep monitoring INR
Lots of drug interactions
120
Q

INR

A

International normalised ratio

Derived from prothrombin time

121
Q

DOAC

A 
New oral anticoag drugs 
Oral
Directly act on factors 2,10 (not via liver, more direct)
No blood tests or monitoring required 
Short half life
Not used in pregnancy 
Used for treatment/thromboprophylaxis 
Only used for INR target ranges of 2-3 (small targets)
122
Q

DVT vs PE mortality

A

PE kills as opposed to DVT

123
Q

Thrombosis

A

Blood coag inside a vessel

124
Q

Thrombosis

A

Arterial - High pressure, platelet-rich - use antiplatelets (aspirin)
Venous - Low pressure, fibrin rich - anticoag (DOACs)

125
Q

Arterial thrombosis - Consequences

A

MI
Stroke
Gangrene

126
Q

MI diagnosis

A

ECG

Cardiac enzymes

127
Q

Peripheral vascular disease diagnosis

A

Ultrasound

Angiogram

128
Q

Arterial thrombosis - Treatment

A 
Aspirin
Clopidogrel 
Prasugrel
Tiglacor 
Anti-platelet
129
Q

Venous thrombosis - Causes

A

Genetic - Antithrombin deficiency, Factor 5 Leiden

Acquired - Anti-phospholipid syndrome (autoimmune)

130
Q

Haemophilia

A

Lack of clotting factors

131
Q

Heparin

A 
Glycoaminoglycan 
Binds to antithrombin and increases its activity
Indirectly inhibits prothrombin
Injected 
Protamine reverses effects of heparin
132
Q

LMW Heparin

A

Smaller molecule

Less variation in dose

133
Q

Aspirin

A

Inhibits cyclo-oxygenase irreversibility
Inhibits thromboxane formation and hence platelet aggregation
Used in arterial thrombosis

134
Q

Clopidogrel

A

Similar to aspirin
Irreversible platelet inhibitor
Target ADP receptor of platelet

135
Q

Pericarditis

A

Cause of acute chest pain

136
Q

Cardiac biomarkers

A

Troponin and CK

137
Q

Pericardial sac

A

lubricates the heart
50ml of fluid
Cardiac tamponade - alteration of fluid level in pericardial sac

138
Q

Acute pericarditis

A

Inflammation of pericardium
With or without pericardial effusion
Features - Chest pain, friction rub, ECG changes, pericardial effusion

139
Q

Pericarditis - Causes

A 
Infectious)
Viral - common - Enteroviruses
Bacterial - uncommon - TB
Non-infectious)
Autoimmune - RA, Sjogrens syndrome 
Neoplastic - Secondary metastatic tumours 
Trauma/iatrogenic - Direct injury
140
Q

Pericarditis - Presentation

A

Chest pain - Severe, sharp, pleuritic, rapid onset, radiates to arm//trapezius ridge, relieved by sitting forward, exacerbated by lying down
Dyspnoea
Cough

141
Q

Pericarditis - Examination

A

Pericardial rub - crunching snow
Sinus tachycardia
Fever
Effusion (pulsus paradoxus)

142
Q

Pericarditis - Investigations

A

ECG - Saddle shaped, ST elevation, PR depression, concave ST segment
Bloods - Raised ESR/CRP, raised troponin, raised WBC
CXR
Echocardiogram

143
Q

Cardiac tamponade - Signs

A

Pulsus paradoxus - Fall in systolic BP of >10mmHg

144
Q

Pericarditis - Management

A

NSAIDs - Aspirin (high dose)

145
Q

Pericarditis - Complications

A

Cardiac tamponade

146
Q

Constrictive pericarditis

A

Calcified pericardium

Treatment - Pericardectomy (surgical removal of pericardium)

147
Q

Pericarditis

A

Bacterial worse than viral

148
Q

Dresslers syndrome

A

Secondary pericarditis with or without pericardial effusion, occurs as a result of injury to the heart

149
Q

Cardiomyopathies

A

Hypertrophic - muscle thickens
Dilated - Heart chambers dilated
Arrhythmogenic - Structural abnormality leading to rhythm disturbances
Diseased desmosomes (adhesion molecules)

150
Q

Hypertrophic cardiomyopathy

A

Diastolic dysfunction
Fibrosis scar tissue
ECG abnormality - Repolarisational T wave inversion, ventricular tachycardia

151
Q

Dilated cardiomyopathy

A

Chamber dilation

Contraction impaired - heart failure

152
Q

Arrhythmogenic cardiomyopathy

A 
Arrhythmias 
Myocyte death - replaced by fibrous fatty tissue
Ventricular 
Epsilon waves 
Diseased desmosomes (adhesion molecules)
153
Q

Naxos disease

A

Palmar plantar caratiderma (hand and foot skin thickened)
Wooly hair
Abnormal ECG - Ventricular arrhythmias
Recessive disease

154
Q

Ion channels abnormalities

A

Voltage-gated
Protein based
Normal heart (asymptomatic) with ECG abnormalities (electrical problem) - Long QT syndrome, brugada syndrome

155
Q

Brugada syndrome

A

Ion channel abnormality

Ajamline test - diagnostic

156
Q

CPVT

A

Catecholaminergic polymorphic ventricular tachycardia

Adrenaline driven - Stress, activity

157
Q

Marfan syndrome

A

Fibrillin disorder
Genetic disorder of connective tissue - tall and thin figure, long arms, legs, fingers and toes
Aortic aneurysms

158
Q

Familial hypercholesterolemia

A 
LDL receptor genetic mutation - not taking up LDL
Vascular disease is a complication 
Heart attack risk increased
Lipid deposition in hands, tendons, eyes
Raised cholesterol
159
Q

Hypertension

A

Treat to reduce risk, not symptoms
Major risk factor for - Stroke, MI, HF, chronic renal disease, AF
Asymptomatic by itself
140/90

160
Q

ABPM

A

Ambulatory blood pressure monitoring

Slightly lower than clinical BP

161
Q

Hypertension - Diagnosis

A

Stage 1 - 140/90
Stage 2 - 160/100
Severe - 180/110

162
Q

Hptn - Treatment

A

Lifestyle

Antihypertensive drug therapy

163
Q

Secondary hptn - Underlying causes

A

Renal

Adrenal

164
Q

Only treat hptn if patient has

A

Target organ damage
CV disease
Renal disease
Diabetes

165
Q

BP targets

A

Under 80 years - 140/90

Over 80 years - 150/90

166
Q

Mechanisms of BP control - Targets for therapy

A

Cardiac output and peripheral resistance
Interplay between RAAS (angiotensin 2) and sympathetic NS (noradrenaline)
Local vascular mediators (constrictors)

167
Q

Vasoconstrictors

A

Angiotensin 2

Noradrenaline

168
Q

ACEi

A

Inhibits ACE, stops production of angiotensin 2
Hptn
Ramipril
Enalapril
Adverse effects - Hypotension, hyperkalaemia, acute renal failure, cough, rash, anaphylaxis
CI - Preg

169
Q

CCB

A

Calcium channel blockers (L type calcium channel blockers)
Hptn, arrhythmias
Amlodipine (dihydropyridine) - Peripheral arterial vasodilators
Verapamil (phenylalkylamines) - Works on heart
Diltiazem (benzothiazepines) - peripheral and heart
Adverse effects (peripheral) - Flushing, headache, oedema, palpitations
Adverse effects (heart) - Bradycardia, AV block

170
Q

BB

A

Hptn
Bisoprolol
Propanolol
Atenolol
Adverse effects - Fatigue, headache, sleep disturbances, bradycardia, hypotension, cold peripheries, erectile dysfunction
Worsens conditions such as asthma, COPD, raynaud’s

171
Q

Aldosterone antagonist

A

Spironolactone

172
Q

ARB

A

Angiotensin 2 receptor blockers (AT1 receptor blocker)
Hptn
Losartan
Valsartan
Adverse effects - Hypotension, hyperkalaemia, renal dysfunction, rash
CI - Preg

173
Q

Beta adrenoreceptor selectivity

A

B1 - Heart (bisoprolol)

B2 - Lungs/airways (propanolol)

174
Q

Diuretics

A

Hptn, HF
Thiazides - distal tubule - Bendroflumethiazide
Loop diuretics - loop of henle - Furosemide
Aldosterone antagonists (Potassium-sparing) - Spironaloctone
Adverse effects - Hypovolaemia, hypotension, metabolic disturbances (low levels of Na, K, Mg, Ca), raised uric acid (lead to gout), erectile dysfunction

175
Q

Alpha-1 adrenoceptor blockers

A

Doxazosin

Treats hptn

176
Q

Hypertension - Treatment order (gold standard)

A

Under 55 - 1) ACEi, 2) CCB, 3)Thiazide, 4) BB/AB/Spironaloctone
Over 55/afro-carib - 1) CCB, 2) ACEi, 3) Thiazide, 4) BB/AB/Spironaloctone

177
Q

Heart failure types

A

LVSD - Left ventricular systolic dysfunction
HFPEP - Diastolic failure
Acute/chronic

178
Q

HF

A

Syndrome of symptoms that suggest impaired efficiency of the heart as a pump
Caused by structural or functional abnormalities of the heart
Common cause - Coronary artery disease

179
Q

HF - drugs

A 
ACEi
ARB
BB
Diuretics (loop)
Aldosterone antagonists
180
Q

HF - Order of treatment

A

1) ACEi + BB (Low doses)
2) Aldosterone antagonists - Spironaloctone
3) ARB (if ACEi is not tolerated)
4) ARNI - Sacubitril/Valsartan
5) Digoxin

181
Q

If ACEi is not tolerated then use an

A

ARB

182
Q

If ACEi + ARB not tolerated then use

A

Hydralazine

183
Q

Nitrates

A

Arterial and venous dilators
Lower BP
Reduce preload+afterload
Used for IHD (Angina) and HF
GTN spray (short-acting) - SE = Syncopy, headache
Isosorbide mononitrate tablets (longer-acting)

184
Q

Chronic stable angina

A 
Anginal chest pain
Predictable 
Exertional, goes away when stop/take GTN
Infrequent 
Stable
185
Q

Unstable angina/NSTEMI

A

Unpredictable
Can be at rest
Frequent
Unstable

186
Q

STEMI

A 
Complete occlusion of artery
Unpredictable 
Rest pain
Persistent 
Unstable
187
Q

Chronic stable angina - Treatment

A

1st line - BB/CCB (either)
2nd line - BB+CCB (both)
3rd line - Long acting nitrate (Isosorbide mononitrate)
Antiplatelets - Aspirin/clopidogrel(if aspirin intolerant)
Statins - Simvastatin/atorvastatin

188
Q

NSTEMI/STEMI - Treatment

A 
Pain relief - GTN spray, diamorphine
Dual antiplatelets - Aspirin+clopidogrel
Antithrombin - Fondaparinux 
Background therapy - BB, ACEi, etc
Surgical - Angioplasty, CABG
189
Q

Antiarrhythmic drugs

A

Na, Ca, K channel targets

190
Q

Vaughan Williams classification - Antiarrhythmic drugs

A

Class 1 - Na channel blockers - Lidocaine
Class 2 - BB - Bisoprolol
Class 3 - Prolong action potential - Amiodarone
Class 4 - CCB - Verapamil

191
Q

Digoxin

A 
Cardiac glycoside - Treats HF
Antiarrhythmic drug - Most commonly used in AF
Inhibits Na/K pump 
Bradycardia, slows AVN
SE - N/V, diarrhoea, confusion
192
Q

HF

A

The inability of the heart to deliver blood (and oxygen) at a rate commensurate with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures
Syndrome of breathlessness, tiredness and fluid overload (systemic/pulmonary oedema) caused by a form of cardiac dysfunction

193
Q

Ejection fraction

A

Percentage of blood leaving your heart each time it contracts

194
Q

HF - Aetiology

A 
MI
Hptn
Cardiomyopathy
Valvular
Endocardial
195
Q

HF - Signs and symptoms

A

Signs - Tachycardia, raised JVP, heart sounds/murmurs, hepatomegaly (pulsatile/tender), peripheral/sacral oedema, ascites
Symptoms - SOB, fatigue, ankle swelling

196
Q

NYHA

A

Class 1-4

Higher class = Severe symptoms

197
Q

HF - Diagnosis

A

Raised NTproBNP - important biomarker in cardiac disease

Echocardiography - to assess structural/functional abnormalities

198
Q

Raised NTproBNP - Causes

A

HF

Plus many other cardiac and non-cardiac conditions

199
Q

Acute HF - Causes

A

Rhythmic disturbances

Viral stress

200
Q

In patients with HF, increased plasma hormone levels of (RAN)

A

Renin
Noradrenaline
Arginine

201
Q

HF with reduced ejection fraction (HFREF) - Gold standard treatments

A

ACEi (k-sparing)
BB - Low dose - Bisoprolol
Aldosterone antagonist - Spironaloctone (K-sparing)

202
Q

ACEi

A

Is not as effective on afro-carib pop as others

203
Q

Blacks with HF - Alternative

A

Isosorbide dinitrate and hydralazine

204
Q

ACEi vs ARB

A

ACEi - dry cough, lower mortality

ARB - no dry cough, greater mortality

205
Q

Ivabradine

A

HF with sinus rhythm

206
Q

NTproBNP - Functions

A

Dilates blood vessel

Opposes Na diuresis

207
Q

Digoxin

A

Slows heart

208
Q

Cardiac resynchronisation therapy (CRT)

A

Multi-site pacing (stimulates ventricles to contract at the same rate)
Treats bundle branch blocks

209
Q

Amiodarone

A

Treats arrhythmias

210
Q

ICD

A

Implanted defibrillators

211
Q

Raised aldosterone

A

Retains Na from blood
Removes K from blood (hypokalaemic)
Commonly due to tumour in adrenals

212
Q

High BP, firstly examine

A

Eyes

213
Q

White coat effect

A

The difference in BP measurement between home and clinical environment

214
Q

Stage 1 hptn - Treatment

A

140 - Only high risk patients

160 - Low risk patients

215
Q

Hypertension treatment effects

A

Reduced headaches and migraines

Otherwise, nothing else is improved

216
Q

BP treatment target ranges

A

140/90

217
Q

Doxazosin

A

Alpha-blocker

218
Q

Hptn - Lifestyle changes

A

1) Weight loss - Diet (salt)
2) Smoking
3) Alcohol

219
Q

Drugs which increase BP

A

SNRI (Selective noradrenaline reuptake inhibitors)
NSAIDs
Oral contraceptive pills
Corticosteroids

220
Q

Stop BP-lowering agents during

A

Surgery

221
Q

ECG provides information on

A

Arrhythmias
Ischaemia
Infarction
Electrolyte disturbances

222
Q

Indications for an ECG

A

Chest pain
Palpitations
Breathlessness
Blackout

223
Q

ECG - Principles

A

Positive deflection is towards the lead/vector
Width of deflection reflects speed of conduction
The amplitude of deflection is related to the mass of myocardium

224
Q

Limb leads - 6

A

1-3
aVR
aVL
AVF

225
Q

Chest leads - 6

A

V1-V6 (Anterior-left lateral)

226
Q

Sinus rhythm

A 
P wave:
Positive) Inferior leads, lead 1
Negative) aVR, biphasic in V1
S wave:
Negative S wave in V1
R wave:
Positive R wave in V6
227
Q

P wave - Abnormalities

A

Low amplitude (Hyperkalaemia, atrial fibrosis)
High amplitude - Tall (Right atrial enlargement)
Wandering pacemaker/focal atrial tachycardia

228
Q

PR interval - Abnormalities

A

Prolonged in AV node disorders

Shorter in young patients

229
Q

QRS complex - Abnormalities

A

Broad - BBB
Small - Pericardial effusion, obesity
Tall - Left ventricular hypertrophy, thin patients

230
Q

QT interval - Abnormalities

A

Long - Low HR

Short - High HR

231
Q

ST segment - Abnormalities

A

Elevated - MI, pericarditis

232
Q

T wave - Abnormalities

A

Inversion - MI

233
Q

Tachycardias

A 
Atrial fib (Irregularly irregular)
Atrial flutter (Rapid, sawtooth atrial pattern)
Supraventricular tachy
Ventricular tachy 
Ventricular fib
234
Q

Ventricular tachy vs ventricular fib

A

Tachy is broader than fib

235
Q

Bradycardia - Causes

A

Conduction tissue fibrosis
Ischaemia
Inflammation
Drugs

236
Q

AV conduction problems

A

1st degree AV block - 1:1 AV ratio
2nd degree AV block 2:1 AV ratio
3rd degree AV block 3+:1 AV ratio
As degree of AV block increases, intervals become longer

237
Q

LBBB

A

Broad QRS

238
Q

LBBB vs RBBB

A

wiLLiam - LBBB

maRRow - RBBB

239
Q

Ischaemia/Infarction

A

T wave flattening inversion
ST depression
ST elevation
Q waves

240
Q

LAD

A

Anterior changes - V2,3,4

241
Q

Circumflex

A

Lateral - 5,6

242
Q

Lateral

A

2,3,5avf (inFERIOR

243
Q

Electrolyte disturbances

A

Hyperkalaemia - Tall T waves, flattened P waves, broad QRS
Hypokalaemia - Flattened T wave, QT prolongation
Hypercalcaemia - Shortened QT
Hypocalcaemia - QT prolongation

244
Q

Electrolyte disturbances

A

Hyperkalaemia - Tall T waves, flattened P waves, broad QRS
Hypokalaemia - Flattened T wave, QT prolongation
Hypercalcaemia - Shortened QT
Hypocalcaemia - QT prolongation

245
Q

Pericarditis

A

Saddle shaped PR depression

ST elevation

246
Q

Ectopic beats

A

Extra beats outside of sinus rhythm

Atrial or ventricular

247
Q

AF - Treatment

A

1st line) BB, CCB, Digoxin

2nd line) Cardioversion (electrical - DC or pharma - Amiodarone)

248
Q

AF increases

A

Stroke risk

249
Q

CHADS-VASC score measures

A

Stroke risk

250
Q

SVT - Treatment

A

Adenosine

Catheter ablation

251
Q

Accessory pathways

A

Pre-excitation (delta waves on ECG)

252
Q

VT - Treatment

A

Catheter ablation

253
Q

BLackout - Treatment

A

Pacemaker

254
Q

Complete heart block - Treatment

A

Pacemaker

255
Q

Diabetes and NSTEMI/STEMI

A

Tend to be without chest pain (silent attack)

256
Q

Biventricular ICD

A

Resynchronises left and right ventricles

Also treats VT episodes

257
Q

PE - ECG changes

A

T wave inversion

258
Q

Valvular heart diseases

A

Aortic stenosis
Mitral regurg
Aortic regurg
Mitral stenosis

259
Q

Aortic stenosis - Types

A

Supravalvular
Subvalvular
Valvular

260
Q

Aortic stenosis - Causes

A

Age-related degenerative calcification
Rheumatic heart disease
IE

261
Q

Bicuspid aortic valve

A

Congenital

262
Q

Aortic stenosis - Pathophysiology

A

Left ventricle becomes exhausted and function declines rapidly

263
Q

Aortic stenosis - Presentation

A

Syncope (extertional)
Angina (increased myocardial oxygen demand - demand/supply mismatch)
Dyspnoea - Breathlessness on exertion

264
Q

Aortic stenosis - Signs

A

Pulsus tardus - slowly rising carotid pulse
Pulsus parvus - decreased carotid pulse amplitude
Heart sounds - S4 gallop due to LVH
Ejection systolic murmur - crescendo-decrescendo character

265
Q

Valvular diseases - Investigations

A

Echocardiography

266
Q

AS - Management

A

Dental hygeine/care - Reduce bacteraemia + IE risk, IE prophylaxis
Surgical replacement
TAVI - Transcatheter aortic valve implantation

267
Q

Mitral regurgitation - Causes

A

IE
Rheumatic heart disease
Mitral valve prolapse

268
Q

MR - Causes

A

Auscultation - Pansystolic murmur

269
Q

MR - Investigations

A

ECG - AF
CXR - LA enlargement
Echo -

270
Q

MR - Management

A

ACEi - vasodilator
IE prophylaxis
Surgical

271
Q

Systolic vs diastolic murmurs

A

Systolic murmurs easier to hear than diastolic murmurs

272
Q

Aortic regurg - Causes

A

Bicuspid aortic valve
Rheumatic
IE

273
Q

AR - Investigations

A

Auscultation - Diastolic blowing murmur,

Wide pulse pressure - High systolic pressure, low diastolic pressure

274
Q

Mitral stenosis

A

V uncommon

275
Q

MS - Causes

A

Rheumatic
IE
Age-related calcification

276
Q

MS - Causes

A

Rheumatic
IE
Age-related calcification

277
Q

IE

A

Infection of heart valve or other endocardial lined structures within the heart (septal defects, pacemaker leads, surgical patches)

278
Q

IE - Types

A 
Left-sided native - (mitral/aortic)
Left-sided prosthetic 
Right-sided native
Device related
Prosthetic
279
Q

IE - Causes

A

Blood infection
Prosthetic heart valve op
Drug abusers (IV)

280
Q

IE - Presentation

A

Signs of systemic infection - Fever, sweats
Embolisation - stroke, pulmonary embolism, MI
Valve dysfunction - HF, arrhythmia

281
Q

IE - Diagnosis

A 
Modified dukes criteria 
Major criteria (2) - Blood cultures, echocardiography - endocarditis, valve leaks
Minor criteria (5) - Predisposing factors, fever, vascular phenomena, immune phenomena, ambiguous blood cultures
282
Q

IE - Peripheral signs

A

Splinter hemorrhages (nails)
Osler’s nodes (tender nodules in fingers)
Embolic skin lesions on hands (from the heart)
Roth spot in eyes

283
Q

IE - Echocardiography

A

TTE - Transthoracic echo (lower quality, non-invasive)

TOE - Transoesophageal echo (better quality, invasive)

284
Q

IE - Diagnosis

A

Blood cultures
Raised CRP
Raised WBC
TTE

285
Q

IE = Treatment

A

IV antimicrobials
Surgical - remove large materials before they embolise, to remove infected devices
Antibiotic prophylaxis

286
Q

IE - Management

A

Blood cultures

Echo

287
Q

IE - most common bacterial cause

A

Strep viridans

288
Q

Right-sided IE - Typical history

A

IV drug abusers, HIV positive

Staph aureus

289
Q

Tetralogy of Fallot - 4 things

A 
Ventricular septal defect
Pulmonary artery stenosis 
Hypertrophy of right ventricle 
Overriding aorta 
Stenosis of the RV outflow leads to RV being at a higher pressure than the left
Hypoxia episodes can then cause death 
Treatment - surgical

Phase 2a NEW (16 decks)

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