Cardiology

Question 1

A negative risk factor for AAA - abdominal aortic aneurysm?

Answer 1

Diabetes but unknown reason

Question 2

Risk factors for AAAs?

Answer 2

Smoking = biggest risk factor
Increasing age
Male
Hypertension
Connective tissue disorders - Ehlers Danos and Marfan syndrome (changes in balance of collagen and elastic fibres)
Family history

Question 3

Pathophysiology for AAA?

Answer 3

Smooth muscle, elastic + structural degredation in all 3 layers of vasuclar tunic (intima, media, adventitia)
All 3 layers = true aneurysm
Not all 3 = pseudoaneurysm (usually due to trauma )
Dilation in AAA typically 3cm+
A dilation that is 5.5cm+ has an increased rupture risk
Rupture = surgical emergency

Question 4

Inflammatory AAA-who affected, causes/associasions, symptoms?

Answer 4

Type that usually affects younger patients and is associated with smoking, atherosclerosis and vasculitis
5-10% of AAAs
Same symptoms + pyrexia (fever)

Question 5

Symptoms of AAA?

Answer 5

Mostly asymptomatic and discovered incidentally
Symptoms generally when ruptured/impending rupture
-sudden epigastric pain radiating to flank
-pulsatile abdominal mass
- tachycardia and hypertension

Question 6

Surface potential signs of AAA?

Answer 6

Grey-Turner’s sign = flank bruising secondary to retroperitneal haemorrhage (also potentially haemorrhagic pancreatitis)

Cullen’a sign = pre-umbilical bruising more associated with acute pancreatitis and ectopic pregnancy but also linked with AAA

Question 7

Primary diagnosis tool for AAA?

Answer 7

Abdominal ultrasound
-fast, cheap, reliable
-highly sensitive and specific

Question 8

Treatment for an asymptomatic aneurysm <5.5cm?

Answer 8

Surveillance + offer advice to manage risk factors (decrease smoking, BMI, BP and statins)

Question 9

Treatment for asymptomatic AAA and >= 5.5cm or >4.0cm and expanded more than 1cm per year?

Answer 9

Elective surgery
Either:
1) EVAR (Endovascular aortic repair) - stent inserted through femoral/iliac artery
-Less invasive but more post op complications

2) open surgery (favoured by nice unless sig comorbidities)
-more invasive but fewer complications

Survival for both=equivalent

(EVAR)

Question 10

Treatment for symptomatic AAA?

Answer 10

Urgent surgical repair (EVAR or open surgery)

Question 11

Treatment for a ruptured AAA?

Answer 11

Stabilise ABCDE, fluids then urgent surgical repair

-Nice says EVAR (Endovascular Aneurysm Repair) preferred in all women, and men over 70 otherwise open surgery preferred
-Do not offer complex EVAR (eg BEVAR) if open surgery is suitable

20% of AAAs rupture anteriorly into peritoneal cavity= poor prognosis
80% rupture posteriorly = better prognosis

100% mortality for ruptured AAA if not treated immediately

Question 12

Cause and treatment for rare AAA in thoracic aorta?

Answer 12

• main cause = marfans/ehlers danos +atherogenesis
• treatment = monitor with CT/MRI or if symptomatic—> surgery immediately

Question 13

Differential diagnosis for AAA?

Answer 13

Acute pancreatitis
Typically non pulsatile + more associated with grey-turner/Cullen signs

Question 14

Define abdominal aortic aneurysm? (AAA)

Answer 14

Permanent aortic dilation exceeding 50% where diameter >3cm
Typically infrarenal (below renal arteries), in elderly men

Question 15

Prevalence of AAA?

Answer 15

1.3 to 12.7% in the uk, most commonly affecting elderly men
Often inherited

Question 16

ECG changes and corrosponding coronary arteries: inferior : ll, lll, avf

Answer 16

right coronary

Question 17

ECG changes and corrosponding coronary arteries: anterior: V3-V4

Answer 17

LAD

Question 18

ECG changes and corrosponding coronary arteries: septal: V1-V2

Answer 18

LAD

Question 19

ECG changes and corrosponding coronary arteries: lateral: l, V5-V6, AVL

Answer 19

Lateral circumflex

Question 20

ECG changes and corrosponding coronary arteries: posterior: V1-V3 (reciprocal ST depression)

Answer 20

Posterior descending

Question 21

Causes of ACS

Answer 21

Acute coronary syndrome

Rupture of atherosclerotic plaque and consequent arterial thrombosis is the main cause

Uncommon causes:
- stress induced cardiomyopathy
- coronary vasospasm without plaque rupture
- drug abuse

Question 22

PCI (coronary artery bypass graft - with stent) and CABG (coronary artery bypass graft) use

Answer 22

STEMI : PCI= ++ CABG= -
NSTEMI : PCI = +++ CABG =+
Stable : PCI = ++ CABG = ++

Question 23

What is troponin?

Answer 23

Protein complex regulates actin:myosin contraction
Highly sensitive marker for cardiac muscle injury
Not specific for acute coronary syndrome
May not represent permanent muscle damage

Question 24

Examples of P2Y12 inhibitors

Answer 24

Clopidogrel
Prasugrel
Ticagelor

Question 25

Why are GPIIb//IIa antagonists used selectively?

Answer 25

Increase risk of major bleeding But still used in combination with aspirin and oral P2Y12 inhibitors in management of patients undergoing PCI for ACS

Question 26

Alternative treatment to PCI for NSTE ACS

Answer 26

CABG used in about 10% of patients But uncommonly, patients may have severe CAD not amenable to revascularisation

Question 27

Pain relief used in ACS management?

Answer 27

Opiates (can delay absorption of P2Y12 inhibitor so only if necessary) Nitrates for unstable angina/coronary vasospasm (GTN spray) (may be ineffective for MI)

Question 28

Clopidogrel vs pasugrel

Answer 28

Pasugrel is much more reliable and useful because it has a direct liver breakdown pathway while clopidogrel effectiveness relies on genetics alongside other factors

Question 29

Ticagrelor vs clopidogrel

Answer 29

Ticagrelor decreases risk of myocardial infarction and cardiovascular death in comparison to clopidogrel

Question 30

What does acute coronary syndromes cover?

Answer 30

Umbrella term for unstable angina, NSTEMI and STEMI

Question 31

How to define different acute coronary syndromes?

Answer 31

Unstable angina- severe ischaemia NSTEMI- partial infarction + Q wave infarction STEMI- transmural infarct and ST elevation in local ECG leads +Non-Q infarction

Question 32

Different acute coronary syndromes pathologies- unstable angina? Occlusion, infarction, ECG, troponins and kinase test result?

Answer 32

Occlusion: partial of minor coronary artery Infarction: no ischaemia only ECG : normal. may show some ST depression/ T wave inversion Troponins + Creatine Kinase MB : Normal

Question 33

Different acute coronary syndromes pathologies- NSTEMI?

Answer 33

Occlusion: major partial/ total minor coronary artery Infarction: sub endothelial infarction (area far away from c.a. occlusion dies) ECG : ST depression + T wave inversion. NO Q waves! Troponins + Creatine Kinase MB : Elevated (increased with infarction)

Question 34

Different acute coronary syndromes pathologies- STEMI

Answer 34

Occlusion: total of major coronary artery Infarction: transmural infarction ECG : ST segment elevation in local leads (2+) Q waves (pathological after some time) Troponins + Creatine Kinase MB : Elevated (increased with infarction)

Question 35

What does an ECG after MI look like?

Answer 35

-hyperacute t wave -pathologically deep q waves - ST segment elevation

Question 36

What’s the difference between types of MI?

Answer 36

T1 = traditional MI due to an acute coronary event (athermatous plaque rupture) T2 = secondary to ischaemia due to either increased oxygen demand or decreased supply (vasopasm, anaemia and sepsis)

Question 37

Is troponin or creatine kinase mb a better indicator of cardiac damage long term?

Answer 37

Troponin has a shorter half life so CKMB is a better biomarker after a few days

Question 38

Pathophysiology of ACS (angina)?

Answer 38

ACS is usually the result of a thrombus—> atherosclerotic plaque formation due to damage to arterial walls causing myocardial ischaemia When a thrombus forms in a fast flowing artery it is made up mostly of platelets. - why anti-platelet medications= key

Question 39

Making a diagnosis of which ACS? (Step by step) (primary investigations)

Answer 39

1) when patient presents with symptoms (eg chest pain) perform ECG 2) ST elevation or new left bundle branch block = STEMI 3) no ST elevation—-> troponin blood tests: - increased troponin + changes (ST depression, t wave inversion or path Q waves) = NSTEMI -normal troponin + no ECG changes then unstable angina or another cause (musculoskeletal chest pain)

Question 40

Symptoms of ACS?

Answer 40

Same as stable angina but pain @ rest prolonged with no relief “impending doom” palpitations and Symptoms more severe

Question 41

Alternative causes of raised troponin?

Answer 41

Gram negative sepsis Myocarditis Aortic dissection Pulmonary embolism Arrhythmias

Question 42

Other investigations when considering ACS?

Answer 42

Those normally arranged for stable angina: - physical examination (heart sounds, signs of heart failure, BMI) - FBC (anaemia) - U&Es (check for electrolyte imbalances prior to ACEi and other meds) -LFTs (prior to statins) -Lipid profile -Thyroid function tests (hypo/hyperthyroid) -HbA1c and fasting glucose (for diabetes) Plus: -chest x ray to investigate other causes of chest pain and pulmonary oedema -Echocardiogram after event to assess for functional damage -Ct coronary angiogram to assess for coronary artery disease

Question 43

Acute management of ACS generally?

Answer 43

MONAC Morphine + anti-emetic (metoclopramide) O2 (if stats <94% or 88-92% if COPD) Nitrates (GTN) Aspirin (300mg) Clopidogrel/Ticagrelor (75mg dual antiplatelet) or pasugrel if undergoing PCI (PY12 inhibitor) Anticoagulant: fondaparinux or heparin *not all patients require oxygen

Question 44

What does GRACE score assess?

Answer 44

Mortality risk of patients with ACS from MI within the next 6 months to 3 years

Question 45

Treatment for low risk NSTEMI/unstable angina

Answer 45

Monitor

Question 46

Treatment for high risk NSTEMI/ unstable angina?

Answer 46

Immediate angiogram and consider PCI

Question 47

Why are diabetics major culprits of Silent MIs?

Answer 47

-diabetic neuropathy -don’t feel the anginal pain and therefore may miss diagnosis and die from sudden collapse

Question 48

Long term and secondary prevention after ACS?

Answer 48

6 As -Atenolol (or other Beta blocker titrated to toleration) (life) -Aspirin (initial dose 300mg -> 75mg life) -Atorvastatin (80mg life) -ACEi (eg ramipril titrated to 10mg) (life) -Another antiplatelet (eg. clopidogrel (75mg for 12months) -Aldosterone antagonist for those with clinical heart failure (ie eplerenone titrated to 50mg once daily) Can add an opiate or GTN spray for pain relief Dual antiplatelet duration will vary following PCI procedures (due to higher risk of thrombus formation in diff stents)

Question 49

Acute complications of ACS (2 >= wk)

Answer 49

Heart failure due to vent fibrillation Mitral incompetence Left ventricle free wall rupture Cardiogenic Shock

Question 50

Other complications of ACS (2< weeks)

Answer 50

Dressler syndrome (autoimmune pericarditis) Heart failure LV aneurysm-heart literally becomes saggy :(

Question 50

How to interpret GRACE score

Answer 50

<5% low risk 5-10% medium risk >10% high risk

Question 50

Complications of MI

Answer 50

DREAD -Death -Rupture of heart septum or Papillary muscles -Edema (Heart failure) -Arrhythmia and Aneurysm -Dressler syndrome embolism, valve disease, recurrence regurgitation, tamponade

Question 50

Flow chart for treatment for NSTEMI or unstable angina

Answer 50

give aspirin 300mg and anticoagulant (fondaparinux or UFH if going for PCI) clinically stable = immediate PCI+ second antiplatelet Low risk = second antiplatelet Intermediate/ high risk = PCI in 72 hours + second antiplatelet

Question 50

Flowchart for STEMI treatment

Answer 50

STEMI diagnosed ---> aspiring 300mg ---> symptom onset <12 h and PCI available in 2h? No ---> ticagrelor (clopdogrel if high bleeding risk)----> fibrinolysis----> failure of fibrinolysis = PCI Yes ---> Prasugrel (clopidogrel if on oral anticoagulent)----> unfractionated heparin, GP IIb/ IIa inhibitor, Bivalirudin----> PCI

Question 50

Initial management of MI

Answer 50

Get in to hospital quickly- 999 call Paramedics-if ST elevation, contact primary PCI centre for transfer Take 300g aspirin immediately Pain relief

Question 51

Risk factors for aortic dissection(AD)

Answer 51

Hypertension = most key Connective tissue disorders (ED,Marfan) Family history of AAA/AD Trauma Smoking

Question 52

Most common location for aortic dissection

Answer 52

Sinotubular junction = where aortic root becomes tubular aorta, near aortic valve (Stanford A)

Question 53

Stanford classification for aortic dissection

Answer 53

A = proximal to left subclavian artery (ascending + arch) (2/3=most common) B = distal to left subclavian artery (descending thoracic) (1/3=less common)

Question 54

Debakey classification of aortic dissection

Answer 54

Type I = originates in ascending aorta and involves at least the aortic arch, but can extend distally Type II = originates and confined to the ascending aorta Type III = originates in the descending aorta and extends distally, but can extend proximally

Question 55

Signs and symptoms of aortic dissection

Answer 55

Symptoms: -Sudden onset ripping/tearing chest pain that may radiate to the back -Syncope (fainting) red flag Signs: -Radio-radial and/or radio-femoral delay -Diastolic murmer due to aortic regurgitation -diff in blood pressure between two arms >10mmHg -hypertension -tachycardia and hypotension (commonly type A)

Question 56

Investigations for diagnosing aortic dissection?

Answer 56

ECG Chest X-ray -may show widened mediastinum >8cm is suspicious Contrast-enhanced CT angiogram (gold standard) -v specific and sensitive and used if patient is hemodynamically stable -shows intima flap, false lumen, dilation of aorta and rupture

Question 57

Investigation in an unstable patient? More for aortic dissection

Answer 57

Transthoracic (TTE) or transoesphageal (TOE) echo TOE is more invasive but more specific for AD and v sensitive -shows intima flap and false lumen -Allows classification of AD as type A or B

Question 57

Treatment for type A aortic dissection

Answer 57

- Blood transfusion - IV labetol (aim for systolic bp 100-120) - Urgent open surgical repair to replace ascending aorta

Question 57

Mortality rate for untreated aortic dissection?

Answer 57

Will result in a false channel rupture and fatal haemorrhage in 50-60% if patients within 24hrs Estimated 20% of patients die before reaching hospital and 30% die before reaching theatre 5 yr survival rate after surgery is 80%

Question 57

Treatment for type B aortic dissection

Answer 57

- conservative management: analgesia and bed rest - IV lavetol (aim for 100-120 systolic bp) - thoracic endovascular aortic repair (TEVAR) may be performed to reduce risk of further dissection yet not standard practice

Question 57

Pathophysiology of aortic dissection?

Answer 57

Surgical emergency!! Tear in intima resulting in blood dissecting through media and separating layers apart -due to mechanical wall stress Creates a false lumen (can propagate forwards and backwards) Abnormal flow can occlude flow through branches of aorta Decreased perfusion to end organs = shock/failure

Question 58

Complications of aortic dissections?

Answer 58

-cardio tamponade -aortic insufficiency (regurgitation) -pre renal AKI -stroke (ischemic)

Question 58

Types of bradycardia

Answer 58

1) RBBB/LBBB (Right bundle branch block ) 2) 1°/2°/3° heart block 3) Sinus bradycardia

Question 58

Two major groups of tachycardia’s

Answer 58

Supraventricular tachycardias AND Ventricular tachycardias

Question 58

Types of supraventricular tachycardias (SVT)

Answer 58

1) AVRT (including WPW) 2) Atrial: -Sinus Tachycardia- Regular -Atrial fibrillation - Irregular -Atrial Flutter - Regular 3) AVNRT (functional) = most common SVT

Question 59

Transmission pathway for heartbeats

Answer 59

SAN -> AVN -> Bundle of His -> Purkinje Fibres

Question 59

Tachycardia vs bradycardia?

Answer 59

Tachycardia = 100< bpm Bradycardia = 60> bpm

Question 60

Is rate control or rythm control preferred?

Answer 60

Rate control is generally preferred and first line for all patients unless they meet specific criteria

Question 60

Causes of atrial fibrillation

Answer 60

Heart failure Hypertension 2° to mitral stenosis Sometimes idiopathic

Question 60

What is atrial fibrillation

Answer 60

Irregularly irregular atrial firing rhythm

Question 60

What is the most common cardiac arrhythmia?

Answer 60

Atrial Fibrillation

Question 61

Risk factors for atrial fibrillation

Answer 61

60+ T2DM Hypertension Valve defects (mitral stenosis) History of MI

Question 62

Pathophysiology of atrial fibrillation

Answer 62

Regular,physiological impulses produced in the sinoatrial node are overwhelmed by the presence of rapid, uncoordinated electrical discharges produced in the atria. -Causes atrial spasm -Atrial blood pools instead of being pumped efficiently to ventricles

Question 63

What does atrial blood pooling cause

Answer 63

Cause a decrease in cardiac output and increased risk of thromboembolic events (particularly stroke)

Question 64

Potential underlying causes of Atrial Fibrillation

Answer 64

Pirates Pulmonary: PE and COPD Ischaemic heart disease: including heart failure Rheumatic heart disease: any valvular abnormality Anaemia, Alcohol, Advancing age Thyroid disease:hyperthyroidism Electrolyte disturbances eg hyper/hypokalaemia Sepsis and sleep apnoea

Question 65

Pathophysiology pathways of atrial fibrillation

Answer 65

(In reality it’s an overlap of these two pathways) triggering event (sepsis and hyperthyroidism) ----> pre - excitation of the atria structural abnormalities (heart failure, valvular abnormalities)----> RAAS activation (increased left atrial pressure) ----> atrial dilation and fibrosis (differences in refractory periods causes electrical re-entry and ectopic foci)

Question 66

Types of atrial fibrillation

Answer 66

1) First episode 2) Paroxysmel : recurrent episodes that stop on their own <7days 3) Persistant: recurrent episodes >7days 4) Permanent: continuous and refractory to treatment so management is aimed at rate control and anticoagulation

Question 67

Symptoms and signs of atrial fibrillation

Answer 67

Symptoms: 1) Palpitations 2) Dyspnoea 3) Chest pain 🚩 4) Syncope 🚩 Signs: 1) irregularly irregular pulse 2) Hypotension 🚩 3) Evidence of heart failure 🚩(eg pulmonary oedema)

Question 68

Investigations to diagnose Atrial fibrillation

Answer 68

ECG: - irregularly irregular pulse - narrow QRS (<120ms) - absent p waves

Question 69

Treatment of atrial fibrillation

Answer 69

Determine if rate or rythm control is more appropriate

Question 70

What is rate control

Answer 70

Rate control accepts the fact that the patient is not in sinus rythm, but aims at controlling the rate to reduce long-term deleterious effects of AF on cardiac function = decrease in heart rate

Question 71

What is rhythm control

Answer 71

Rythm control aims to restore normal sinus rythm, “cardioversion”, can be either electrical or pharmalogical =restore normal PQRS shape

Question 72

When is rate control recommended for atrial fibrillation

Answer 72

Onset > 48 hours or unknown

Question 73

When is rhythm control recommended for atrial fibrillation?

Answer 73

- younger age - onset <48 hours - no underlying heart disease - reversible cause of AF - Failure of rate control - Haemodynamic instability acutely

Question 74

Treatment for atrial fibrillation if patient is haemodynamically unstable

Answer 74

Emergency electrical synchronised DC cardioversion

Question 75

Treatment of atrial fibrillation if patient is haemodynamically stable?

Answer 75

Onset of AF <48hrs: rate or rythm control Onset of AF >48hr/unknown: rate control and anticoagulation for at least three weeks Then offer rythm control if unsuccessful or still symptomatic

Question 76

First line drugs for rate control

Answer 76

Beta-blocker OR rate limiting CCB (Calcium channel blockers) Bispropolol OR diltiazen or verapamil Second line is to combine drugs

Question 77

Pharmacological treatments for rhythm control

Answer 77

- Flecainide or amiodarone

Question 78

Electrical treatments for rhythm control

Answer 78

Synchronised DC shock starting at 150J under shirt acting general anaesthesia

Question 79

Pathway for atrial fibrillation treatment

Answer 79

< 48 hours onset = rate or rhythm control >48 hours onset or unknown = rate control and anticoag for 3 weeks (minimum)---> then consider rhythm control Adverse features = rhythm control : electrical cardioversion ---> rhythm control: pharmacological cardioversion

Question 80

What does the CHA2DS2-VASc assess?

Answer 80

Assess stroke risk (once you’ve already had AF) and therefore the anticoagulation need for Atrial fibrillation

Question 81

Scoring criteria for CHA2DS2-VASc score

Answer 81

Congestive heart failure Hypertension Age 75=< (2) DM Stoke (2) Vascular disease Age 65-74 Female Total: 1 unless female then 2=< then oral coagulation required

Question 82

Complications of atrial fibrillation

Answer 82

Heart failure Ischaemic stroke Mesenteric ischeamia

Question 83

What is an atrial flutter

Answer 83

Irregular organisers atrial firing ~250-350bpm Less common and less severe than AF

Question 84

Pathophysiology of atrial flutter

Answer 84

Fast atrial ectopic firing (250-350bpm) causes atrial spasm, but not as uncoordinated as A-Fib. Pathway typically from opening of tricuspid valve

Question 85

Symptoms of atrial flutter

Answer 85

Dyspnoea Palpitations

Question 86

Investigations to diagnose atrial flutter

Answer 86

ECG : (diagnostic) f wave “saw tooth” pattern Often with a 2:1 block (2 p waves for every QRS)

Question 87

Treatment of acutely unstable atrial flutter

Answer 87

DC synchronised cardioversion

Question 88

Treatment of stable atrial flutter

Answer 88

Rythm/rate control with oral anticoagulation (prevent thromboemboli) Also radiofreq ablation

Question 89

What the most common supraventricular tachycardia?

Answer 89

AVNRT (functional)

Question 90

Pathophysiology of AVNRT

Answer 90

Re-entrant pathway goes through AVN

Question 91

Treatment for AVNRT

Answer 91

Same as AVRT (WPW)

Question 92

What is an AVRT?

Answer 92

AVRT ( Atrioventricular reciprocating tachycardia) -> an accessory pathway exists for impulse conduction, not re entry through AVN Often Hereditary

Question 93

Most common example of an AVRT

Answer 93

Wolff-Parkinson White syndrome (WPW)

Question 94

Pathophysiology of WPW

Answer 94

Accessory pathway for conduction= Bundle of Kent A pre excitation syndrome (excites ventricles earlier than typical pathway so that’s why you see delta waves)

Question 95

Symptoms of WPW

Answer 95

Palpitation Dizziness Dyspnoea

Question 96

Investigations to diagnose WPW

Answer 96

Ecg: 1) slurred delta waves 2) short PR interval 3) wide QRS

Question 97

Treatment for WPW

Answer 97

First line: Valsalva manoeuvre (Forceful exhalation against a closed airway.. close nose and mouth and breath hard like ur trying to pop ur ears) This triggers nerves to slow down electrical signals in the heart Carotid massage 2nd line: if 1st unsuccessful IV Adenosine (will temporarily cease conduction; when patient feels like dying) 6mg, then 12mg, then further 12mg (additional doses if 6mg is unsuccessful) Can also consider surgical radiofrequency ablation of bundle of Kent

Question 98

What is long QT syndrome?

Answer 98

Ventricular tachycardia Typically congenital channelopathy disorder where mutation affects cardiac ion channels and therefore heart conduction QT interval 480ms+

Question 99

Causes of long QT syndrome

Answer 99

-Romano ward syndrome (autosomal dominant) -Jervell - lang - Nielsen syndrome (autosomal recessive) -Hypokalemia + hypocalcemia (non-inherited) -Drugs (Amiodarone,magnesium)

Question 100

What is ventricular fibrillation?

Answer 100

Shapeless rapid auscultations on ECG Patient becomes pulseless + goes into cardiac arrest (no effective cardiac output) 1st line treatment-> electrical defibrillation But unsynchronised as patient is pulseless

Question 101

What is torsades de pointes?

Answer 101

-Polymorphic ventricular tachycardia in patients with prolonged QT -Rapid irregular QRS complexes which “twist” around baseline - can cease spontaneously or develop to ventricular fibrillation

Question 102

Heart sound S2?

Answer 102

Aortic + Pulmonary close

Question 103

Heart sound S3?

Answer 103

Shows RAPID VENTRICULAR FILLING in early diastole * normal in young/pregnant * pathological in mitral regurgitation + heart failure

Question 104

Heart sound S4?

Answer 104

Pathological “gallop” * due to blood forced in to stiff hypertrophic ventricle (LVH + aortic stenosis)

Question 105

What does P represent on a normal ECG?

Answer 105

Atrial depolarisation

Question 106

What does PR interval represent on a normal ECG?

Answer 106

AVN conduction delay

Question 107

Average length of PR interval?

Answer 107

0.12-0.2s

Question 108

What does QRS interval represent?

Answer 108

Ventricle depolarisation + atrial repolarisation

Question 109

Average length of a QRS interval?

Answer 109

0.08-0.1s 0.12=< is abnormal

Question 110

Why does ST segment represent on a normal ECG?

Answer 110

Isovolemic ventricular relaxation

Question 111

What does T represent on a normal ECG?

Answer 111

Ventricular repolarisation

Question 112

What are ECGs useful in diagnosing?

Answer 112

-MI (STEMI, NSTEMI) -Arrhythmias -Electrolyte disturbance: K+, CA++ -Pericarditis -Chamber hypertrophy -Drug toxicity (eg. digoxin)

Question 113

Scale for ECG paper?

Answer 113

0.5 mV for 1 big square amplitude and 0.2 seconds time small square = 0.1mV and 0.04 s

Question 114

ECG leads for RCA

Answer 114

aVF + II + III (Inferior)

Question 115

ECG leads for LAD

Answer 115

V1-V4 (Anterior + septal)

Question 116

ECG leads for LCx

Answer 116

V5 + V6 + aVL + I (Lateral)

Question 117

Heart sound S1?

Answer 117

Mitral + Tricuspid close

Question 118

What is cardiac tamponade

Answer 118

Accumulation of a large vol of fluid in the pericardial space (pericardial effusion) that begins to impair ventricle filling

Question 119

Cause of Cardiac tamponade

Answer 119

Typically pericarditis Hence risk factors are all pericarditis related

Question 120

Symptoms of cardiac tamponade

Answer 120

Related to pericarditis

Question 121

Signs of cardiac tamponade

Answer 121

Beck’s triad: - hypotension (reduced cardiac output) - raised JVP (heart failure) - muffled heart sounds Pulses paradoxes: systolic bp reduction of >10mmHg on inspiration

Question 122

Primary investigations to diagnose cardiac tamponade

Answer 122

ECG: may show electrical alternations - varying QRS amplitudes due to heart bouncing back and forth in pericardial fluid CXR - chest x ray : big globular heart ECHO: diagnostic tool

Question 123

Treatment for cardiac tamponade

Answer 123

Urgent therapeutic pericardiocentesis - needle inserted between xiphisternum and left costal margin and directed towards left shoulder -sometimes done under ultrasound guidance -pericardial fluid aspirated to relieve intrapericardial presure

Question 124

Main symptom of arrhythmogenic cardiomyopathy

Answer 124

Arrhythmia

Question 125

What do all cardiomyopathies carry a risk of?

Answer 125

Arrhythmias

Question 126

Likely cause of sudden cardiac death in a young person?

Answer 126

Often due to an inherited condition Most likely a cardiomyopathy or ion channelopothy

Question 127

Cause of arrhythmogenic hypertrophy

Answer 127

Desmosome gene mutations

Question 128

What is the most common cardiomyopathy in general

Answer 128

Dilated cardiomyopathy

Question 129

Cause of dilated cardiomyopathy

Answer 129

-Autosomal dominant familial inheritance (cytoskeleton gene mutation) -IHD -Alcohol

Question 130

Pathophysiology of dilated cardiomyopathy

Answer 130

Thin cardiac walls poorly contract leading to a decrease in CO LV/RV or 4 chamber dilation and dysfunction

Question 131

Symptoms of dilated cardiomyopathy

Answer 131

-Shortness Of Breath -heart failure (usually) -atrial fibrillation -thromboemboli

Question 132

Investigations to diagnose dilated cardiomyopathy

Answer 132

ECG ECHO

Question 133

Treatment for dilated cardiomyopathy

Answer 133

Treat underlying condition Eg Atrial fibrillation, heart failure

Question 134

Epidemiology of hypertrophic cardiomyopathy

Answer 134

Affects 1 in 500 people

Question 135

What is LVOT?

Answer 135

Left ventricular outflow tract obstruction is a recognised feature of hypertrophic cardiomyopathy

Question 136

Three types of cardiomyopathy?

Answer 136

1) Hypertrophic 2) Restrictive 3) Dilated

Question 137

What are cardiomyopathies?

Answer 137

Diseases of the myocardium (Muscular/conduction defects)

Question 138

What is the most common cardiac cause of death in young people?

Answer 138

Hypertrophic cardiomyopathy

Question 139

Causes of hypertrophic cardiomyopathy

Answer 139

Familial -inherited mutation of sarcomere proteins — troponin T and Myosin B

Question 140

Pathophysiology of of hypertrophic cardiomyopathy

Answer 140

Thick non compliant heart = impaired diastolic filling => decrease in CO

Question 141

Symptoms of hypertrophic cardiomyopathy

Answer 141

May present with sudden death Chest pain/angina Palpitations SOB Syncope/dizzy spells

Question 142

Investigations to diagnose hypertrophic cardiomyopathy

Answer 142

Confirm with abnormal ECG ECHO (diagnostic) Genetic testing

Question 143

Treatment for hypertrophic cardiomyopathy

Answer 143

Beta blocker CCB Amiodarone (anti-arrhythmic)

Question 144

What is the cause of inherited arrhythmia? (Channelopothy)

Answer 144

Caused by ion channel protein gene mutations

Question 145

Which ions do cardiac channelopathies relate to?

Answer 145

Potassium Sodium Calcium

Question 146

Examples of cardiac channelopothies?

Answer 146

Long QT Short QT Brugada CPVT

Question 147

Cardiac channelopothies effect on heart structure?

Answer 147

No effect- have a structurally normal heart

Question 148

Symptom of cardiac channelopothy?

Answer 148

Syncope

Question 149

QT prolonging drugs?

Answer 149

Many drugs on this list that may be used to treat other conditions eg some antidepressants But they can kill people with long QT syndrome

Question 150

SADS sudden arrhythmic death syndrome?

Answer 150

Usually refers to normal heart/arrhythmia

Question 151

Familial hypercholesterolaemia (FH)?

Answer 151

Inherited abnormality of cholesterol metabolism

Question 152

What does familial hypercholesterolaemia lead to?

Answer 152

Serious premature coronary and other vascular diseases

Question 153

Aortavascular syndromes

Answer 153

Marfan Loeys-Dietz Vascular Ehler Danos

Question 154

What type of inheritance are inherited cardiac conditions usually?

Answer 154

Dominantly inherited Offspring have a 50% chance of inheritance

Question 155

Why is screening important for inherited cardiac conditions?

Answer 155

Genetic testing is available Risk (arrhythmic death, vascular dissection) needs to be assessed for each individual Life saving treatments are available (ICD, beta blockers, statins, vascular surgery) Lifestyle modifications can save lives

Question 156

Why is screening for inherited cardiac conditions highly contentious?

Answer 156

Because long QT has only a 1/5000 prevalence so it will very rarely be picked up and not a huge benefit to it in the normal population But for first degree relatives- 1/2 chance of it being passed on so highly recommended

Question 157

What investigations need to be done as part of a hypertension screening?

Answer 157

Urine dipstick (kidneys = end organ damage) ECG (LVH) HBA1c Renal function Fundosocopy (eyes) Lipid profile Qrisk Only check cortisol if there’s a secondary cause of hypertension

Question 158

What do you need to calculate Qrisk?

Answer 158

Lipid profile

Question 159

What changes in the arteries are likely to be seen due to angina?

Answer 159

-Smooth muscle proliferation and migration from the tunica media to the intima -decreased release of nitric oxide - infiltration of Subendothelial space by low-density lipoprotein (LDL) particles - formation of foam cells from macrophages

Question 160

Which blood test is the most accurate marker for acute cardiac damage?

Answer 160

Troponin T - short term, released by cardiac myocytes

Question 161

Blood marker for heart failure?

Answer 161

Brain natriuretic peptide

Question 162

Inflammatory blood marker?

Answer 162

C reactive protein (CRP)

Question 163

Which investigation is diagnostic for heart failure?

Answer 163

Echocardiogram- allows you to see ventricles and valves (valves cause murmurs)

Question 164

Which medication can be prescribed to relieve symptoms (swollen ankles) of heart failure?

Answer 164

Oral digoxin (cardiac glycoside)

Question 165

Which two medications can cause postural hypertension?

Answer 165

Bisproplol Amlodipine

Question 166

Non pharmacological treatment to help with postural hypertension?

Answer 166

Increase salt intake Increase oral fluid intake Compression stockings Sit + stand slowly

Question 167

What is postural hypertension?

Answer 167

Sustained reduction of systolic blood pressure of at least 20 mmHg or diastolic blood pressure of 10 mmHg within 3 minutes of standing

Question 168

Causes of postural hypersensitivity?

Answer 168

Disorders affecting autonomic nervous system (eg. Parkinson’s disease) reduced blood volume, or iatrogenic causes eg. Antihypertensives

Question 169

Pharmovological treatment options of postural hypertension?

Answer 169

Oral fludrocortisone

Question 170

Prevalence of postural hypertension?

Answer 170

Affects 5% to 30% of people aged over 65 years and up to 60% of people with Parkinson’s disease

Question 171

5 investigations to assess for infective endocarditis?

Answer 171

Bedside- ECG, urinalysis Bloods - FBC, CRP, blood cultures Imaging - Echo

Question 172

Low amplitude p wave possible causes?

Answer 172

Atrial fibrosis Obesity Hyperkalemia

Question 173

High amplitude p waves possible cause?

Answer 173

Right atrial enlargement

Question 174

Broad notched ‘bifid’ p wave possible causes?

Answer 174

Left atrial enlargement

Question 175

Broad QRS possible causes?

Answer 175

Ventricular conduction delay/ branch bundle block Pre-excitation

Question 176

Small QRS complex possible causes?

Answer 176

Obese patient Pericardial effusion Infiltrative cardiac disease

Question 177

What can T wave changes indicate?

Answer 177

- ischeamia/infarction - myocardial strain (hypertrophy) - myocardial disease (cardiomyopathy)

Question 178

Ecg for ischeamia?

Answer 178

T wave flattening inversion ST segment depression

Question 179

How common is restrictive cardiomyopathy

Answer 179

Rare

Question 180

Causes of restrictive cardiomyopathy

Answer 180

-Granulomatous disease (sarcoidosis,amyloidodis) -idiopathic -post MI-fibrotic

Question 181

Pathophysiology of restrictive cardiomyopathy

Answer 181

Rigid fibrotic nyocardium fills poorly and contracts poorly => decreased CO

Question 182

Symptoms of restrictive cardiomyopathy

Answer 182

Severe: -dyspnoea -S3 + S4 sounds -oedema -congestive heart failure -narrow pulse pressure ( normally 120/80 but here it’s 105/95 and consequently blood stasis due to the decreased gradient)

Question 183

Investigations to diagnose restrictive cardiomyopathy

Answer 183

ECG ECHO cardiac catheterisation (diagnostic)

Question 184

Treatment for restrictive cardiomyopathy

Answer 184

None Consider transplant Patients typically die within 1yr

Question 185

Break down the word atherosclerosis

Answer 185

Atheroma= fatty deposits in artery walls Sclerosis= process of hardening or stiffening of blood vessels

Question 186

What is atherosclerosis caused by?

Answer 186

Chronic inflammation and activation of the immune system in the artery wall which causes deposition of lipids

Question 187

What three things do fibrous atheromous plaques lead to?

Answer 187

1. Stiffening - leads to hypertension and strain of heart pumping against resistance 2. Stenosis - leads to reduce blood flow (eg. Angina) 3. Plaque rupture- giving off a thrombus that blocks a distal vessel leading to ischaemia (eg. Acute conorary syndrome)

Question 188

Atherosclerosis modifiable risk factors

Answer 188

1. Smoking 2. Alcohol consumption 3. Poor diet (High sugar and trans-fat and reduced fruit and vegetable and omega 3 consumption) 4. Low exercise 5. Obesity 6. Poor sleep 7. Stress

Question 189

Medical co-morbidities that increase the risk of atherosclerosis

Answer 189

1. Diabetes 2. Hypertension 3. Chronic kidney disease 4. Inflammatory conditions (rheumatoid arthritis) 5. Atypical antipsychotic medications

Question 190

End result of atherosclerosis?

Answer 190

1. Angina 2. Myocardial infarction 3. Transient ischaemic attacks 4. Stroke 5. Peripheral vascular disease 6. Messenteric ischaemia

Question 191

Two types of prevention of cardiovascular disease?

Answer 191

1. Primary prevention - for patients that have never had cardiovascular disease in the past 2. Secondary prevention - for patient that have had angina, myocardial infarction, TIA, stroke or peripheral vascular disease

Question 192

How to optimise modifiable risk factors?

Answer 192

1. Advice on diet, exercise and weight loss 2. Stop smoking 3. Stop drinking alcohol 4. Tightly treat co-morbities (diabetes)

Question 193

Primary prevention of cardiovascular disease?

Answer 193

1. Perform a Q-risk 3 score 2. Over 10% risk of having heart attack or stroke in the next ten years? Offer a statin (Current NICE = atorvastatin 20mg at night) 3. All patients with CKD or type 1 diabetes for more than ten years should also be offered atorvastatin 20mg

Question 194

Nice guidelines to statin prescription?

Answer 194

1. check lipids at 3 months- aim for increasing dose to aim for 40% reduction in non-HDL Cholesterol- always check adherence first! 2. Check LFTs within 3 months and at 12 months, don’t need to be checked again if normal 3. Statins can cause a transient and mild raise in ALT and AST in first few weeks of use and don’t need stopping if rise is less than 3 times the upper limit of normal

Question 195

Secondary prevention of cardiovascular disease?

Answer 195

4 As: Aspirin (plus second anti platelet like clopidogrel for 12months) Atorvastatin 80mg Atenolol (or other beta-blocked - commonly bispropol - titrated to maximum tolerated dose) ACE inhibitor (commonly ramipril) (tritated to max tolerated dose)

Question 196

Notable side effects of statins

Answer 196

1. Myopathy (check creative kinase in patients with muscle pain or weakness) 2. T2DM 3. Haemorrhagic strokes (very rarely) Usually benefits far outweigh risks and newer statins are mostly very well tolerated

Question 197

What’s a Q-risk 3 score?

Answer 197

-Predicts risk of CVD in 10 upcoming years -Factors include: Age SBP BMI Socieconomic status Ethnicity -Score of ten plus (10% + risk in the next ten years) is an indication to start 1° lipid lowering therapy (statins)

Question 198

What is atorvastatin an example of?

Answer 198

Lipid lowering therapy

Question 199

Two types of bundle branch block?(BBB)

Answer 199

RBBB right LBBB left

Question 200

Causes of RBBB

Answer 200

Pulmonary emboli IHD VSD

Question 201

Causes of LBBB

Answer 201

IHD Valvular Disease

Question 202

Pathophysiology of RBBB?

Answer 202

RV later activation than LV

Question 203

Pathophysiology of LBBB?

Answer 203

LV activation later than RV

Question 204

Atherosclerosis non-modifiable risk factors

Answer 204

1. Older age 2. Family history 3. Male

Question 205

ECG presentation of RBBB?

Answer 205

MaRRoW M in v1 (RSR wave) W in v6 (seep S wave) Wide: physiological S2 splitting (heart sound)

Question 206

ECG presentation of LBBB?

Answer 206

WiLLiaM W in V1 M in V6 Reversed S2 splitting

Question 207

What is a bundle branch block?

Answer 207

Blocks of bundles of His

Question 208

What is a 1° AV block?

Answer 208

PR interval prolongation (200ms+) Every P is followed by a QRS

Question 209

Symptoms of 1° heart block?

Answer 209

Asymptomatic

Question 210

Treatment of 1° heart block

Answer 210

No treatment as it is mild

Question 211

Causes of 1° heart block

Answer 211

Drugs (Bb, CCB, digoxin —> block AVN conduction)

Question 212

The difference between different degrees of heart block?

Answer 212

Severity 1° may not cause symptoms 2° sometimes troublesome symptoms 3° most serious = medical emergency

Question 213

What is 2° heart block?

Answer 213

When some p waves are conducted but others aren’t

Question 214

Two types of 2° heart block

Answer 214

Mobitz I (Weinkebach’s) Mobitz II

Question 215

What is Mobitz I?

Answer 215

PR prolongation until a QRS is dropped (PR interval progressively elongates). Can eventually drop a beat occasionally.

Question 216

Causes of Mobitz I?

Answer 216

Same as 1° heart block (Bb, CCB, Digoxin) Inferior MI

Question 217

Treatment of Mobitz I?

Answer 217

No treatment unless symptomatic eg syncope Treatment—> pacemaker

Question 218

Symptoms of Mobitz I?

Answer 218

May have syncope

Question 219

What is Mobitz II?

Answer 219

PR interval consistently prolonged (not progressively enlarging) with random dropped QRS

Question 220

Causes of Mobitz II?

Answer 220

Drugs, Inferior MI, Rheumatic fever

Question 221

Symptoms of Mobitz II?

Answer 221

Syncope SOB Chest pain

Question 222

Treatment for Mobitz II?

Answer 222

Pacemaker

Question 223

What is 3° heart block?

Answer 223

AV dissociation (complete heart block; atria + ventricles beat independently of each other) * ventricular ESCAPE rythm is sustaining heartbeat —> SAN (best) if dysfunctional, AVN takes over —> if dysfunctional ventricle pacemakers take over (worst, firing rate 20-40bpm)

Question 224

Causes of 3° heart block

Answer 224

Acute MI Hypertension Structural heart disease

Question 225

Treatment for 3° heart?

Answer 225

IV atropine + permanent pacemaker

Question 226

Management of cor pulmonale?

Answer 226

Management involves treating the symptoms and underlying cause Long term oxygen therapy often used Prognosis is poor unless reversible underlying cause

Question 227

Define hypertensive heart disease?

Answer 227

Heart failure and conduction arrhythmias due to unmanaged high blood pressure

Question 228

What if patients are intolerant to ACEi and ARB? (Heart failure)

Answer 228

Hydralazine/nitrate combination

Question 229

Main phenotypes of heart failure

Answer 229

HF with reduced ejection fraction (HFrEF) HF with preserved ejection fraction (HFpEF) HF due to severe valvular heart disease (HF-VHD) HF with pulmonary hypertension (HF-PH) HF due to right ventricular systolic dysfunction (HF-RVSD)

Question 230

Define heart failure

Answer 230

Inability for heart to deliver O2 blood to tissues at a satisfactory rate for the tissues metabolic requirements * a syndrome not a diagnosis

Question 231

Cause of heart failure?

Answer 231

IHD Cardiomyopathy Valvular disease Cor pulmonale Anything that increases cardiac work: -obesity -htn -pregnancy -hyperthyroid -arrhythmias

Question 232

Risk factors for heart failure

Answer 232

Age (65+) Smoking Obesity Previous MI Male

Question 233

Pathophysiology for Cor pulmonale?

Answer 233

RH failure due to disease of lungs +/ pulmonary vessels Increased pressure and resistance in pulmonary arteries results in right ventricle being unable to pump blood out Leads to back pressure of blood into right atrium, the vena cava and the systemic venous system

Question 234

Pathophysiology of heart failure

Answer 234

-Failing hearts = decreased CO due to dysfunctional frank starling law 1- compensatory mechanism activation —Raas + sns initially works (=increase BP) Increases aldosterone + ADH Increases ADR / NaD 2- soon compensation fails and heart undergoes cardiac remodelling (decreased CO) in response to compensation * heart less adapted to function so increase in RAAS + SNS will exacerbate fluid overload * heart failure affecting both L+R circuits = congestive heart failure

Question 235

Normal physiology of heart

Answer 235

Normally- increased preload= increased afterload= increased cardiac output (frank starling law)

Question 236

Three ways heart failure can be classified?

Answer 236

1) Time classified 2) Acute or chronic 3) Ejection fraction classified

Question 237

How is heart failure ejection fraction classified?

Answer 237

Normal = 50–70% > 50% = preserved Diastolic failure (filling issues) Eg. Hypertrophic cardiomyopathy, LVH (aortic stenosis) < 40% = reduced Systolic failure (pump issues) Eg. IHD - ischaemic tissue

Question 238

What does LHS failure result in?

Answer 238

Pulmonary vessel backlog —> pulmonary oedema

Question 239

What does RHS failure result in?

Answer 239

Systemic venous backlog —> peripheral oedema

Question 240

3 cardinal non specific symptoms of heart failure

Answer 240

SOBASFAT 1 Shortness of breath 2 Ankle swelling 3 Fatigue

Question 241

Other symptoms of heart failure

Answer 241

-orthopnoea (dyspnoea worse lying flat) -increased JVP -bibasal crackles (pul oedema) -hypotensive -tachycardic

Question 242

NY heart association class 1-4 of HF severity

Answer 242

1 no limit on physical activity 2 slight limit on moderate activity 3 marked limit on moderate + gentle activity 4 symptoms even at rest

Question 243

Methods of diagnosing of heart failure?

Answer 243

Bloods ECG Chest X-ray ECHOcardiogram - gold standard

Question 244

Blood results with heart failure?

Answer 244

BNP (brain natriuretic peptide) = key marker High >400ug/ml Level correlates with extent of damage So more severe heart failure = higher bnp It is released from stressed ventricles in response to increase mechanical stress *might also measure NT ProBNP (inactive BNP) and levels are 5x higher so increase of >2000 ug/ml

Question 245

ECG results with heart failure?

Answer 245

Abnormal Eg evidence of LVH

Question 246

Chest x ray results with heart failure

Answer 246

ABCDE Alveolar bat wing oedema B-lines Cardiomegaly Dilated upper lobe vessels Effusion (pleural)

Question 247

Purpose of echocardiogram?

Answer 247

Assess heart chamber dimensions

Question 248

Conservative treatment for heart failure

Answer 248

Lifestyle changes: Decrease bmi Exercise Stop smoking + alcohol

Question 249

First line treatment for chronic heart failure

Answer 249

ABAL First line: -ACEi (eg ramipril titrated up to tolerated dose of 10mg) -Beta blocker (eg bisoprolol titrated up to 10mg) Add in: -Aldosterone antagonist when symptoms not controlled with A and B (eg spironactone or eplerenone) -Loop diuretic improves symptoms (eg. Furosemide 40mg once daily) *consider desynchronisation therapy (improves A-V coordination) - low dose and slow uptitration is key with ACEi and Bb

Question 250

Surgical treatments for heart failure?

Answer 250

Revascularisation Valve surgery Heart transplant (last resort)

Question 251

What if ace inhibitors are not tolerated?

Answer 251

ARB like candersartan titrated go 32mg can be used instead

Question 252

What should patients have monitored when on diuretics, ace inhibitors and aldosterone antagonists?

Answer 252

U&E All three medications cause electrolyte disturbances

Question 253

Patients with valvular heart disease should avoid which drug?

Answer 253

Ace inhibitors unless indicated by a specialist

Question 254

Respiratory causes of cor pulmonale?

Answer 254

-COPD is most common cause -pulmonary embolism -interstitial lung disease -cystic fibrosis -primary pulmonary hypertension

Question 255

Presentation of Cor Pulmonale

Answer 255

Patients often asymptomatic Main presenting complaint is shortness of breath (Also caused by chronic lung disease) May also present with peripheral oedema, increased breathlessness of exertion, syncope or chest pain

Question 256

Signs of Cor Pulmonale

Answer 256

-Hypoxia -cyanosis -raised JVP (due to backlog of blood in jugular veins) -peripheral oedema -third heart sound -murmurs (eg pan-systolic in tricuspid regurgitation) -hepatomegaly due back pressure in the hepatic vein

Question 257

Primary vs secondary hypertension

Answer 257

1° = Essential hypertension (idiopathic/no known cause) 95% cases 2° = known underlying cause 5% cases

Question 258

Causes of secondary hypertension

Answer 258

- Renal disease (CKD-most common cause due to diabetic nephropathy) - Endocrine disorders (phaeochromocytoma, conn’s, cushing’s) - Medication/iatrogenic : glucocorticoids, ciclosporin, atypical antipsychotics, combined oral contraceptive pill -pregnancy

Question 259

Non modifiable risk factors for hypertension

Answer 259

Non modifiable risk factors for hypertension

Question 260

Modifiable risk factors for hypertension

Answer 260

Obesity Sedentary lifestyle Alcohol excess Smoking High sodium intake (>1.5g a day) Stress

Question 261

Define the limits for stages of hypertension

Answer 261

(H) = clinic reading (A) = ambulatory Discrepancy of >= 20/10mmHg between clinic and ambulatory suggests “white-coat hypertension 1 = 140/90 (H), 135/85 (A) 2= 160/100 (H), 150/95 (A) 3 = 180 and/ or 110 <

Question 262

Malignant (accelerated) hypertension?

Answer 262

Severe increase in blood pressure >=180/120 mmHg (stage 3) with signs of retinal haemorrhage and/or pailloedema, associated with target organ damage = emergency assessment and treatment

Question 263

Pathophysiology of hypertension

Answer 263

Ultimately all mechanisms will increase RAAS and SNS activity (CO) and TPR => increase in BP as BP=COxTPR

Question 264

Signs of malignant hypertension

Answer 264

Hypertensive retinopathy Visual disturbances Cardiac symptoms eg chest pain Oliguira or polyuria Overall rare but scary and unrelated to cancer just very severe symptoms

Question 265

Symptoms of hypertension

Answer 265

Mostly asymptomatic and found in screening May have pulsatile headache, classically occipital and worse in the morning

Question 266

Signs of hypertension to consider

Answer 266

Signs of the underlying cause of secondary hypertension Eg phaeochromocytoma, hyperthyroidism or Cushing’s

Question 267

How to diagnose hypertension

Answer 267

If bp reading in hospital is between 140/90 and 180/120 mmHg then offer ABPM to confirm diagnosis -bp is measured for 24h with at least 2 measurements per hour during waking hours -overall at least 14 measurements are required <135/85 = not hypertensive > 135/ 85 = stage 1 hypertension - treat if < 80 years and any of: target organ damage, diabetes, established CVD, renal disease, Qrisk > 10% -then other medication to treat hypertension > 150/95 = stage 2 hypertension - treat all patients regardless of age -then other medication to treat hypertension

Question 268

Other investigations for hypertension?

Answer 268

Assess end organ damage (more damage = worse prognosis) : - Fundoscopy: assess for hypertensive retinopathy - 12- lead ECG: assess for LVH - Urinalysis and ACR: assess for renal dysfunction + diabetes risk - Bloods: HbA1c, U&Es, total cholesterol, HDL cholesterol

Question 269

Treatment guidelines for hypertension

Answer 269

If age <55 years or T2 diabetes ---> ACE in (or ARB if intolerant) then offer ACE in + CCB or ACE in + thiazide like diuretic----> then all three if needed. if k+ > 4.5 add alpha or beta blocker if K+ < 4.5 add spironolactone If age >55 years or Afro Caribbean then CCB ---> then offer ACE in + CCB or ACE in + thiazide like diuretic----> then all three if needed. if k+ > 4.5 add alpha or beta blocker if K+ < 4.5 add spironolactone if <80 aim for <140/90 > 80 years aim for <150/90 CKD: aim for <140/90 CKD and DM <130/80

Question 270

If a patient has T2DM and is black or 55+, would they take CCB or ACEi?

Answer 270

T2DM takes precedence and they should take ACEi BUT ARBs are preferred for black patients so that might be preferable

Question 271

Complications for hypertension?

Answer 271

Heart failure Increased IHD risk CKD/Renal failure PVD Dementia Increased risk of cerebrovascular incident

Question 272

What reduction do you expect with a full dose of any single drug?

Answer 272

Systolic: 8-10mmHg Diastolic: 4-6mmHg

Question 273

Thresholds for treatment for hypertension?

Answer 273

Low CVD risk 160/100mmHg High CVD risk 140/90mmHg (Clinic thresholds)

Question 274

Targets for blood pressure after treatment?

Answer 274

- Routine <140/90 mmHg - Previous stroke < 130/80mmHg - Heavy proteinuria <130/80mmHg - CKD and Diabetes <130/80mmHg - older patients <150/90mmHg

Question 275

How many drugs are generally needed to control blood pressure?

Answer 275

Mostly one or two

Question 276

Can you lower blood pressure with lifestyle changes?

Answer 276

Yes: -Weight loss -Salt restriction -Exercise -Alcohol

Question 277

Why would blood pressure treatment be withheld?

Answer 277

During general anaesthesia hypotension can be a problem and anyihypertensives block attempts to increase BP ==> ACEi + ARBs temporarily stopped

Question 278

Limits for diagnosing hypertension

Answer 278

>= 140/90 mmHg in clinic >= 135/85 mmHg at home (ambulatory blood pressure monitoring)

Question 279

Two most common causes of infective endocarditis

Answer 279

1) S.aureus- most common overall + associated with IV drug use and prosthetic heart valves => increased virulence, Sx onset in days-weeks = ACUTE 2) S.viridans- second most common + usually affects a native valve and associated with poor dental hygiene => decreased virulence, Sx onset in weeks-months = SUBACUTE

Question 280

Catergorisations of endocarditis

Answer 280

1) Acute 2) Subacute 3) Non- bacterial thrombotic ‘marantic’ - non-infective cause of endocarditis secondary to thrombus formation on the valvular surface - associated with malignancy or SLE (Libman-Sacks endocarditis)

Question 281

Other less common causes of infective endocarditis

Answer 281

S. Bovis (associated with colon cancer) S. Epidermis (associated with in dwelling lines and prosthetic valves) HACEK organsisms (usually culture -ve) - Haemophilus - Aggregatibacter - Cardiobacterium - Eikenella - Kingella

Question 282

Risk factors for infective endocarditis

Answer 282

Male 2.5x Elderly with prosthetic valve Young IV drug user Young with congenital heart defect Rheumatic heart disease

Question 283

Which valves are more commonly affected by Infective endocarditis

Answer 283

Mitral valve most commonly affected overall Tricuspid valve is most associated with IV drug use

Question 284

Pathophysiology of infective endocarditis

Answer 284

- any cause of abnormal endocardium —> turbulent blood flow and thrombus formation (platelets) - thrombus can get infected due to bacterial source - bacterial colonisation of the thrombus —> formation of vegetations —> valvular damage -typically happens around valves -causing regurgitation => aortic and mitral insufficiency and increase risk of heart failure

Question 285

Symptoms of infection endocarditis

Answer 285

Rather vague -Fever or chills -headache -SOB -night sweats, fatigue, weight loss -joint pain (might be due to septic emboli)

Question 286

Signs of infective endocarditis

Answer 286

1) Osler nodes (painful nodules on fingers\toes) 2) Janeway lesions (painless placques on palms and soles) 3) splinter haemmorrhages (red plum lines under nails) 4) Roth’s spots: white centred retinal haemorrhages *heart murmer +- signs of heart failure*

Question 287

Primary investigations for infective endocarditis

Answer 287

-ECG (prolonged PR interval=aortic root abscess) -Blood cultures - 3 sets in 24 hours BEFORE ANTIBIOTICS -Inflammatory markers (CRP) - eg raised ESR\CRP + neutrophillia -FBC -ECHO: TOE more invasive than TTE but much more sensitive and specific = gold standard -Urinalysis

Question 288

What is the modified Duke Criteria

Answer 288

Requires 2 major criteria, or 1 major and 3 minor, or 5 minor criteria for diagnosis of infective endocarditis

Question 289

Major Duke Criteria for infactive endocarditis

Answer 289

- 2 positive blood cultures - ECHO TOE shows endocardia’s involvement Eg. Vegetations , abscess or regurgitation

Question 290

Minor Duke criteria for infective endocarditis

Answer 290

-predisposing heart condition -IVDU -Fever >38°C -1 +ve blood culture -immunological phenomenon (Osler’a nodes, Roth’s spots or rheumatoid factor) -vascular abnormalities (eg. Septic/arterial emboli, pulmonary infarct)

Question 291

First line treatment for infective endocarditis

Answer 291

IV antibiotics for 4 weeks following nice guidelines, extended to 6 weeks for prosthetic valves -local guidelines should be followed with nice antibiotic guidance. General antibiotic ideas? General: Amoxycillin, gentamicin, vancomyocin and rifampicin Staphylococci: flucloxacillin, vancomyocin, rifampicin, gentamicin Streptococci: benzylpenicillin Enterococci: amoxicillin HACEK : cefrtriaxone

Question 292

Second line treatment for infective endocarditis

Answer 292

Surgery: aim to remove infected tissue and repair it replace affected valves

Question 293

Complications of infective endocarditis

Answer 293

Congestive heart failure Septic embolisation Valvular rupture or fistula Aortic root abscess

Question 294

What is infective endocarditis

Answer 294

Infection of endocardium: - an abnormal endocardium - bacterial source —> vegetation

Question 295

Environmental exacerbating factors for IHD

Answer 295

Exercise Cold weather Heavy metals Emotional stress

Question 296

Physiology of IHD

Answer 296

Myocardial ischemia occurs when there is an imbalance between heart’a oxygen demand and supply, usually from an increase in demand accompanied by limitation of supply: 1) impairment of blood flow by proximal arterial stenosis 2) increased distal resistance eg. Left ventricular hypertrophy 3) reduced oxygen-carrying capacity of blood eg. Anaemia

Question 297

What is microvascular angina (syndrome X)

Answer 297

‘ANOCA’ Angina with apparently normal (main) coronary arteries Females mostly Cause unknown

Question 298

Which risk factor drastically increases incidence of IHD

Answer 298

Age

Question 299

Symptoms that don’t associate with angina

Answer 299

No fluid retention (unlike heart failure) Palpitation (not usually) Syncope or pre-syncope (very rare)

Question 300

How to assess chest pain?

Answer 300

OPQRST Onset Position (site) Quality (nature/character) Relationship (with exertion, posture, meals, breathing and with other symptoms) Radiation Relieving or aggravating factors Severity Timing Treatment

Question 301

Differential diagnosis for myocardial ischemia

Answer 301

Pericarditis/myocarditis Pulmonary embolism/pleurisy Chest infection/ pleurisy Gastro-oesophageal (reflux/spasm/ulceration) Musculoskeletal Physcological

Question 302

Treatment for myocardial ischemia

Answer 302

Reassure Lifestyle - smoking - weight - exercise - diet Advice for emergency Medication Revascularisation

Question 303

Advantages and limitations of CT angiography (fuzzier than normal angiography)

Answer 303

Good diagnostic test and at spotting severe disease Not so good at moderate disease Anatomical, not functional

Question 304

Advantages and drawbacks to exercise testing

Answer 304

Good functional test Relies on patients ability to walk on a treadmill (useless for elederly, obese, arthritis etc)

Question 305

Side effects of beta blockers

Answer 305

Tiredness, nightmares Erectile dysfunction Bradycardia Cold hands and feet

Question 306

Contraindication for beta blockers?

Answer 306

Asthma- do not give

Question 307

Side effect of aspirin

Answer 307

Gastric ulceration

Question 308

Pros and cons of PCI

Answer 308

Pro: - less invasive - convenient - repeatable - acceptable Cons: - risk stent thrombosis - can’t deal with complex disease - dual antiplatelet therapy

Question 309

Pros and cons of CABG

Answer 309

Pros: - prognosis - deals with complex disease Cons: - invasive - risk of stroke - can’t do if frail - one time treatment -time for recovery

Question 310

Which veins can a CABG use?

Answer 310

Internal mammary artery (from chest) Saphenous vein (from leg)

Question 311

If you don’t get chest pain when you run.. how likely is IHD?

Answer 311

Very low probability

Question 312

Side effect of GTN spray?

Answer 312

Excruciating headache

Question 313

Reasons for imperfect blood supply to the heart?

Answer 313

- Atherosclerosis - Thrombosis - Thromboemboli - Artery spasm - collateral blood vessels - blood pressure/ cardiac output/ heart rate - Arteritis

Question 314

Which arteries does atherogenesis affect most commonly?

Answer 314

LAD Circumflex RCA

Question 315

Risk factors for IHD

Answer 315

Age Smoking Obesity, high serum cholesterol Diabetes Hypertension Family history M>F Cocaine use Stress Physical inactivity

Question 316

Symptoms of stable angina pain?

Answer 316

1. Central crushing chest pain radiating to neck/jaw 2. Brought on with exertion 3. Relieved with 5mins rest or GTN spray

Question 317

Four types of angina?

Answer 317

1. Stable - normal three point definition 2. Unstable - pain at rest, not relieved by inactivity or GTN spray + no ECG CHANGES 3. Prinzmetal’s - due to coronary vasospasm (not due to cv vessel atherogenesis) Seen increasingly in cocaine users ECG shows ST elevation 4. Decubitus - induced when lying flat (usually complication of cardiac failure)

Question 318

Fibrous cap in stable angina?

Answer 318

Fibrous cap is strong and less rupture prone

Question 318

Patholophysiology of ischaemic heart disease?

Answer 318

Atherogenesis: Endothelial injury attracts cells to site via chemokines (IL1, IL6, IFN-Y) 1. Fatty streak = Foam cells (lipid laden macrophages) and T-cells 2. Intermediate lesions = foam cells (bigger as taken up more lipid), t- cells and smooth muscle cells Platelets also aggregate and adhere to site inside vessel lumen 3. Fibrous plaques (advanced) = large lesions (foam cells, t-cells, smooth muscle, fibroblasts, lipids with a necrotic core) Develops a fibrous cap over lesion

Question 319

What happens if plaque is prone to rupture?

Answer 319

Prothrombotic state, platelet adhesion and accumulation leads to progressive luminal narrowing

Question 320

Difference between ischaemia and infarction?

Answer 320

Ischaemia= blood flow restricted Infarction= lumen fully occluded

Question 321

When do symptoms for stable angina start?

Answer 321

When 70 to 80% lumen occluded Due to poiseulle’s law, nothing much happens until the diameter stenosis reaches 70% and then there is rapid decline

Question 322

Symptoms of IHD?

Answer 322

Central crushing chest pain radiating to jaw/neck, worsens with time (doesn’t peak straight away ) NSFD: Nausea Sweating Fatigue Dyspnoeic weak breathing + hypotensive/tachycardic in ACS and “impending sense of doom” and palpitations

Question 323

How to diagnose stable angina?

Answer 323

1st line= ECG- resting and with exercise (to induce ischaemia) Coronary angiography- looks for stenoses and atherosclerotic arteries (~70-80% occluded) Gold standard but invasive so not first line

Question 324

Treatment for stable angina?

Answer 324

-Symptomatic= GTN sublingual spray -Lifestyle modifying (decrease weight, stop smoking, exercise, diet etc) -Pharmacological (all patients=1st line) 1. CCB (CI heart failure) or B-b (CI Asthma) Switch if either is not tolerated If both are contraindicated or not tolerated, other drugs to consider as monotherapy: - a long acting nitrate (isorbide monitrate) - nicorandil - ivabradine - ranolazine Secondary anti platelet treatment is recommended (75mg aspirin) (eg if they have a stent but not necessarily for stable angina) Potentially Revascularisation: PCI/CABG with an MDT meeting or coronary angiogram if symptoms not controlled

Question 325

Exacerbating factors for IHD

Answer 325

Supply: -Anemia -hypoxemia Demand: -hypertension -tachycardia -valvular heart disease

Question 326

Epidemiology of pericarditis?

Answer 326

- males - 20-50yrs

Question 327

Causes of pericarditis

Answer 327

1) Usually idiopathic 2) Or caused by a virus: - most common cause = coxsackievirus - mumps - EBV - VZV - HIV Less common causes: - bacterial - TB - systemic autoimmune disorders - malignancy - trauma

Question 328

Pathophysiology of pericarditis

Answer 328

- inflamed pericardial layers rub against each other = more inflammation -cause exudate and adhesions within pericardial sac 1) may stay dry (no extra fluid needed to compensate for friction) 2) develop pericardial effusion (extra fluid) - if it becomes large enough to affect heart function = cardiac tamponade

Question 329

Symptoms of pericarditis

Answer 329

Sudden onset sharp, pleuritic chest pain which can spread to left shoulder tip (phrenic) - Relieved by sitting up or leaning forward - Worse laying flat *may have signs of rhs failure due to constructive pericarditis -> SOB, peripheral oedema and tachycardia

Question 330

Sign of pericarditis

Answer 330

Pericardial friction rub on auscultation - heard at left sternal edge as patient leans forward - squeaky leather “to and fro” sound

Question 331

Differential diagnosis of pericarditis

Answer 331

Most key to rule out MI - central crushing chest pain not related to lying down - no pericardial rub

Question 332

What is constructive pericarditis

Answer 332

- granulation tissue formation in pericardium means impaired diastolic filling as it becomes thickened and hardened - late complication of pericarditis - sign of poor prognosis—> congestive heart failure - commonly associated with TB

Question 333

Primary investigations to diagnose pericarditis

Answer 333

ECG: widespread saddle shaped ST-elevation (sensitive) and PR depression (specific) CXR: may show “water bottle” heart = pericardial effusion - pneumonia commonly seen in bacterial pericarditis Transthoracic ecg: to exclude pericardial effusion or tamponade ESR and CRP: might increase due to inflammation Troponin will be daisies if there’s an element of concomitant myocarditis

Question 334

Treatment for idiopathic or viral pericarditis

Answer 334

1st line: NSAIDs + Colchine 2nd line: NSAIDs + Colchine + low-dose prednisolone

Question 335

Treatment for bacterial pericarditis

Answer 335

IV antibiotics and pericardiocentesis with washout, culture and sensitivities

Question 336

Complications of pericarditis

Answer 336

1) Pericardial effusion—> cardiac tamponade 2) Myocarditis 3) Constrictive pericarditis

Question 337

Prognosis of pericarditis

Answer 337

Majority of cases (viral and Idiopathic) are self limiting, whereas bacterial (purulent) pericarditis can be fatal if untreated.

Question 338

Another name for pericarditis?

Answer 338

Dressler syndrome

Question 339

What is pericarditis?

Answer 339

Typically acute (can be chronic); inflammation of pericardium +/- effusion -pericardium has two layers and innervated by phrenic hence inflammation results in pain

Question 340

What is PVD?

Answer 340

Peripheral vascular disease is essentially reduced blood supply and ischaemia in the lower limbs due to atherosclerosis and thrombosis in the arteries

Question 341

Risk factors for PVD?

Answer 341

Smoking = single greatest risk factor T2DM Ageing Males affected at younger age Obesity Hypertension CKD

Question 342

Three main patterns of presentation of PVD?

Answer 342

1. Intermittent claudication (least severe) 2. Critical limb ischaemia 3. Acute limb-threatening ischaemia (most severe)

Question 343

Intermittent claudication?

Answer 343

Reflects an inadequate increase in skeletal muscle perfusion during exercise - atherosclerotic partial lumen occlusion - pain on exertion

Question 344

Critical limb ischaemia?

Answer 344

Advanced form of chronic limb ischaemia - big occlusion and blood supply barely adequate to meet metabolic demand - pain at rest - risk of gangrene/infection

Question 345

Acute limb-threatening ischemia?

Answer 345

Most commonly caused by emboli, usually cardiac origin, resulting in sudden decrease in limb perfusion - total vessel occlusion - emboli tend to lodge at bifurcations or sudden narrowing

Question 346

Symptoms of acute limb-threatening ischemia

Answer 346

6Ps Pulselessness Pallor Pain Perishingly cold Paralysis Paresthesia - present in chronic limb ischemia too but more you have=more limb threatening - all 6 = deadly!!

Question 347

What happens when BV supplying region is occluded?

Answer 347

1) irreversible nerve damage (within 6h) 2) irreversible muscle damage (6-10h) 3) skin changes are last to appear =>likely gangrenous

Question 348

Fontaine classifications of PVD

Answer 348

I) asymptomatic II) intermittent claudication- aching or burning of leg muscles -stage IIa = after 200m walking -stage IIb = after less than 200m walking Relieved within minutes of rest III) critical limb ischaemia - pain at rest + night IV) tissue loss: ulceration or gangrene

Question 349

Why might symptoms be masked in PVD?

Answer 349

Inability to walk (eg severe heart failure) Pain insensitivity (eg diabetic neuropathy)

Question 350

Signs to look for in PVD?

Answer 350

-Low ABPI (<0.9) or lack of lower leg pulse -Skin changes on leg (ulceration, thin, shiny, discolouration -Buerger’s test +ve -Bruits: pulsatile regions due to turbulent blood flow (aortic, femoral, carotid) -Some of 6Ps

Question 351

Buerger’s test?

Answer 351

1) lie patient flat 2) elevate leg to 45° for 1 min 3) positive = pallor then reactive hyperaemia

Question 352

Primary investigations for PVD?

Answer 352

1) ABPI (ankle-brachial blood pressure index) 0.8-1.3 normal 0.5-0.8 intermediate claudication <0.5 critical limb ischaemia Pulse absent = acute limb-threatening ischaemia 2) duplex ultrasound imaging- assess location and severity of stenosis 3) ECG, U+E, FBC, HbA1c - assess cardiovascular risk *Ct angiography if surgery considered, not routine as more invasive*

Question 353

Treatment of intermittent claudication

Answer 353

RF management: -Supervised exercise programme if available (2 hrs per week for three months) -or if not then unsupervised exercise training -smoking cessation -bp control -diet and weight management -statins -HbA1c control -antilplatelets If 3 months exercise doesn’t improve quality of life then consider Revascularisation surgery

Question 354

Treatment of chronic limb ischaemia

Answer 354

Revascularisation surgery (PCI if small, bypass if larger) Amputation if severe

Question 355

Treatment for acute limb threatening ischeamia

Answer 355

Surgical emergency Revascularisation within 4-6hrs otherwise increased amputation risk

Question 356

Complications of PVD

Answer 356

Amputation Ulceration + gangrene Permanent limb weakness Infection and poor tissue healing Increased risk of cerebrovascular accidents + CVD

Question 357

Another name for peripheral vascular disease? (PVD)

Answer 357

Peripheral arterial disease (PAD)

Question 358

The main indications for ACEi?

Answer 358

Hypertension Heart failure Diabetic neuropathy

Question 359

Examples of ACEi?

Answer 359

Ramipril Enalapril Perindopril Trandolapril (Largely do the same job but vary in price)

Question 360

Main side effects of ACEi?

Answer 360

Due to reduced angiotensin II formation: - hypotension - acute renal failure - hyperkalemia - teratogenic effects in pregnancy Due to increased kinins: - cough - rash - anaphylactoid reactions

Question 361

Main clinical indications for ARBs?

Answer 361

-Hypertenison -Diabetic Neuropathy -Heart failure (when ACEi contraindicated)

Question 362

Examples of ARBs?

Answer 362

Cadersartan (most common) Losartan Val sar tan Irbesartan Telmisartan

Question 363

Main side effects of ARBs?

Answer 363

Symptomatic hypotension Hyperkalemia Potential for renal function Rash Angioedema Generally very well tolerated

Question 364

Contraindication of ARBs?

Answer 364

Pregnancy

Question 365

Main clinical indications of CCBs?

Answer 365

Hypertension ischaemic heart disease - angina Arrrhythmia (tachycardia)

Question 366

Examples of CCBs?

Answer 366

Amlodipine Diltiazem Verapamil Felodipine Lacidipine Nifedipine

Question 367

Dihydropyridines CCBs?

Answer 367

Nifedipine Amlodipine Felodipine Lacidipine Preferentially affect vascular smooth muscle = peripheral arterial vasodilators

Question 368

Phenylyalkylamines CCBs?

Answer 368

Verapamil Main effects in the heart = negatively chronotropic and inotropic

Question 369

Benzothiazepines CCBs?

Answer 369

Diltiazem = immediate heart/peripheral vascular effects

Question 370

Main side effects of peripheral vasodilation? (CCBs)

Answer 370

Flushing Headache Oedema Palpitations

Question 371

Main side effects due to negatively chronotropic effects? (CCBs)

Answer 371

Bradycardia Atrioventricular block

Question 372

Main side effects due to negatively ionotropic effects? (CCBs)

Answer 372

Worsening of cardiac failure

Question 373

Side effect of verapamil?

Answer 373

Constipation

Question 374

Main clinical indications for Bb?

Answer 374

Ischaemic heart disease - angina Heart failure Arrhythmia Hypertension

Question 375

Examples of B1 selective Bb?

Answer 375

Metoprolol Bisoprolol

Question 376

An example of a less selective B1 Bb?

Answer 376

Atenolol

Question 377

B1/B2 (non-selective) Bb examples?

Answer 377

Propranolol Nadolol Carvedilol

Question 378

Are beta 1 selective blockers absolute?

Answer 378

Selectivity is relative rather than absolute

Question 379

What percentage of beta adrenoreceptors in the heart are actually B1?

Answer 379

Only 60% 40% are B2 =hence you can’t use the term cardioselective to describe B1 selective beta blockers

Question 380

Main side effects of Bb?

Answer 380

Fatigue Headache Sleep disturbance/ night mares Bradycardia Hypotension Cold peripheries Erectile dysfunction

Question 381

Contraindications of Bb?

Answer 381

Worsening of : - asthma (can be severe) or COPD - PVD - claudication or raynauds - Heart failure - if given in standard dose or acutely

Question 382

Main clinical indications of Diuretics?

Answer 382

Hypertension Heart failure

Question 383

4 classes of diuretics?

Answer 383

1) thiazides and related drugs (distal tubule) 2) loop diuretics (loop of henle) 3) potassium-sparing diuretics 4) aldosterone antagonists

Question 384

Examples of thiazide and related diuretics?

Answer 384

Bendroflumethiazide Hydroclorothiazide Chlorthalidone

Question 385

Examples of loop diuretics?

Answer 385

Furosemide Bumetanide

Question 386

Examples of potassium-sparing diuretics

Answer 386

Spironalactone Eplerenone Amiloride Triamterine

Question 387

Main side effects of loop diuretics

Answer 387

Hypovolemia Hypotension

Question 388

General side effects of diuretics?

Answer 388

Hypokalemia Hyponatremia Hypomagnesaemia Hypocalcemia Hyperuricaemia- gout

Question 389

Side effects of thiazides?

Answer 389

Erectile dysfunction Impaired glucose tolerance

Question 390

Other anti hypertensives?

Answer 390

A-1 adrenoceptor blockers (Doxazosin) Centrally acting anti-hypersensitive (Moxonidine + methyldopa) Direct renin inhibitor (Aliskeren)

Question 391

What do nitrates do?

Answer 391

Arterial and venous dilators Reduction of preload and afterload Lower BP

Question 392

Main clinical indications for nitrates?

Answer 392

Ischeamic heart disease - angina Heart failure

Question 393

Main examples of nitrates

Answer 393

Isorbide mononitrate GTN spray GTN infusion

Question 394

Main side effects of nitrates

Answer 394

Headache due to GTN syncope (spray)

Question 395

Drug for antiplatelet therapy in angina if aspirin intolerant?

Answer 395

Clopidogrel

Question 396

Example of an antiarrhythmic drug?

Answer 396

Digoxin

Question 397

Drug class and mechanism of Digoxin?

Answer 397

Class: Cardiac glycoside Inhibits Na/K pump and causes: - bradycardia - slows AVN conduction - increased ectopic activity - increased force of contraction

Question 398

Side effects of digoxin?

Answer 398

Narrow therapeutic range Nausea Vomiting Diarrhoea Confusion

Question 399

Main clinical indication of Digoxin?

Answer 399

Atrial fibrillation to reduce ventricular rate response Severe heart failure as +vly ionotropic

Question 400

Why treat hypertension?

Answer 400

Important preventable cause of premature morbidity and mortality Major risk factors for: - stroke (ischaemic and haemorrhagic) - myocardial infarction - heart failure - cognitive decline - premature death Increases risk of Atrial fibrillation as well

Question 401

Cause of rheumatic fever

Answer 401

Systemic response to B haemolytic group A strep (Strep pyogenes) Typically pharyngitis

Question 402

Rheumatic heart disease?

Answer 402

In 50% of cases of rheumatic fever it goes on to affect the heart

Question 403

Histological appearance of rheumatic fever

Answer 403

Valves affected show Aschoff Bodies

Question 404

Pathophysiology of rheumatic fever

Answer 404

M protein from S. pyogenes reacts with valve tissue of the heart Antibodies vs this “cross-link” results ins auto-antibody mediated destruction +- inflammation Molecular Mimicry!! * mostly affects the mitral valve (70% just mitral and 25% mitral and aortic) Typically thickens leaflets causing mitral stenosis

Question 405

Symptoms of rheumatic fever

Answer 405

- New murmur (esp mitral stenosis) - Syadenham’s chorea (neurological disorder that results in uncoordinated jerky movements) - arthritis - Erythema nodosum (swollen fat causing red patches\bumps) - pyrexia - evidence of strep A infection

Question 406

Investigations to diagnose rheumatic fever

Answer 406

CXR= cardiomegaly/ heart failure (signs of mitral stenosis) ECHO= details extent of valvular damage

Question 407

Jone’s criteria for diagnosis of rheumatic fever

Answer 407

1) recent S. pyogenes infection AND 2) 2 major signs (new murmur, arthritis, erythema nodosum, syndham chorea) OR 3) 1 major + 2 minor (pyrexia, increased ESR/CRP, arythalgia)

Question 408

Treatment for rheumatic fever

Answer 408

Antibiotics- IV benzyloenicillin STAT, then phenoxypenicillin for 10days

Question 409

Treatment for Sydenham’s chorea

Answer 409

Haloperidol

Question 410

Epidemiology of rheumatic fever

Answer 410

Almost exclusively in developing countries only In young people

Question 411

Symptoms of anaphylactic

Answer 411

Hypotension Tachycardia Urticaria Puffy face flushing of cheeks

Question 412

Treatment of anaphylactic shock

Answer 412

ABCDE IM adrenaline (SNS activation=stress response)

Question 413

Cause of anaphylactic shock

Answer 413

Due to IgE mediated Type 1 hypersensitivity vs allergen -Histamine release causes construction -causes excess vasodilation and bronchoconstriction Hypoxic!

Question 414

What is shock

Answer 414

A medical emergency- life threatening -hypoperfusion -due to acute circulation failure -leads to tissue hypoxia and risk of organ dysfunction

Question 415

What are the five different types of shock?

Answer 415

- Cardiogenic (heart pump failure) - Distributive (arterial supply to tissues): 1) septic 2) neurogenic 3) anaphylactic - Hypovolemic (affects venous return to heart and therefore preload)

Question 416

Presentation of shock

Answer 416

1) decreased urine output 2) reduced GCS (Glasgow coma scale) 3) Skin - pale , cold, sweaty, vasoconstriction - increased capillary refill time = earliest, most accurate indicator - takes 3+ seconds for hand to turn pink after pressed for 5seconds 4) confusion 5) pulse- weak + rapid 6) prolonged hypotension = can lead to life threatening organ failure AFTER acute emergency recovery

Question 417

Key organs at risk of failure from shock?

Answer 417

Kidneys Lungs Heart Brain

Question 418

Cause of cardiogenic shock

Answer 418

Due to heart pump failure; MI, cardiac tamponade, pulmonary emboli

Question 419

Symptoms of cardiogenic shock

Answer 419

Heart failure signs (oedema) Increased JVP S4

Question 420

Treatment of cardiogenic shock

Answer 420

ABCDE Treat underlying cause

Question 421

Causes of hypovolemic shock

Answer 421

1) Blood loss - trauma, GI bleed 2) Fluid loss- dehydration

Question 422

Symptoms of hypovolemeic shock

Answer 422

Clammy pale skin Confusion Hypotension Tachycardia

Question 423

Treatment of hypovolemic shock

Answer 423

ABCDE Airways Breathing (give O2) Circulation (IV fluids)

Question 424

Cause of neurogenic shock

Answer 424

Due to spinal cord trauma eg RTA Results in disrupted SNS, but intact PSNS

Question 425

Symptoms of neurogenic shock

Answer 425

Hypotension Bradycardia Confused Hypothermic

Question 426

Treatment for neurogenic shock

Answer 426

ABCDE IV Atropine (Blocks vagal tone: allows more psns inhibition, more chance for SNS to work)

Question 427

Cause of septic shock

Answer 427

Due to uncontrolled bacterial infection

Question 428

Symptoms of septic shock

Answer 428

Pyrexia (high temp.) warm peripheries Tachycardic

Question 429

Treatment for septic shock

Answer 429

ABCDE Broad spectrum antibiotic

Question 430

Pathophysiology of atrial septal defect

Answer 430

Shunt of blood L->R and therefore not cyanotic (blue skin inducing) - increased flow to right side of heart and lungs - may overload RHS circulation causing RVH - (Right ventricular hypertrophy (RVH) is a pathologic increase in muscle mass of the right ventricle in response to pressure overload,)

Question 431

Investigations to diagnose an atrial septal defect

Answer 431

ECHO

Question 432

Treatment for atrial septal defect

Answer 432

Sometimes there is spontaneous closure Otherwise treatment is surgical Percutaneous (key hole technique)

Question 433

Clinical signs of atrial septal defects

Answer 433

Pulmonary flow murmur Big pulmonary arteries on CXR Big heart on chest x ray Risk of infective endocarditis

Question 434

Another name for atrial septal defect

Answer 434

Patent foramen ovale

Question 435

What is an atrioventricular septal defect?

Answer 435

Essentially a hole down the middle of heart (no atrial or IV septum!) Can be complete or partial

Question 436

What is atrioventricular septal defect associated with

Answer 436

Massively associated with Downs Syndrome

Question 437

Symptoms of atrioventricular septal defect

Answer 437

Dyspnoea Exercise intolerance Complete defect: - breathless new pats with poor weight gain and feeding and needs repair wishing is surgically challenging Partial defect: Can present late in adulthood band can be left alone if no right heart dilation

Question 438

Prognosis of atrioventricular septal defect

Answer 438

Progresses to eventually Eisenmenger’s and hard to treat

Question 439

Most common congenital heart defect?

Answer 439

Bicuspid aortic valve 1-2% of the population M>F

Question 440

Is the aortic valve bicuspid or tricuspid?

Answer 440

Typically tricuspid

Question 441

Disadvantage of bicuspid aortic valve?

Answer 441

Bicuspid degenerates quicker than normal and will become regurgitative earlier Are also associated with coarction and dilation of ascending aorta Can be severely stenotic in infancy or childhood

Question 442

Pathophysiology of coarctation of aorta

Answer 442

Aorta narrows at or just distal to ductus arteriosus => blood diverted massively through aortic arch branches = increased perfusion in upper body vs lower body

Question 443

Symptoms of coarction of aorta

Answer 443

Scapular bruits from collateral vessels Hypertension in collaterals (right arm) Murmur

Question 444

Investigations to diagnose coarctation of aorta

Answer 444

CXR: “notched ribs” dilated intercostal vessels CT angiogram

Question 445

Treatment of coarctation of aorta

Answer 445

Surgical repair or stenting of stenoses segment, even when mild to prevent long term problems

Question 446

Long term problems of coarctation

Answer 446

-Re coarctation requiring repeat intervention -Aneurysm formation at the site of repair Hypertension leads to: - early coronary artery disease/stroke - sub arachnoid haemorrhage

Question 447

What is coarction of the aorta associated with?

Answer 447

Turner’s syndrome and Berry aneurysms of the brain

Question 448

Prevalence of patent ductus arteriosus

Answer 448

10-20%

Question 449

What is patent ductus arteriosus

Answer 449

When ductus arteriosus fails to close post birth = unusual

Question 450

Pathophysiology of patent ductus arteriosus

Answer 450

Blood shunt from aorta to pulmonary trunk -risk of pulmonary overload and Eisenmenger’s

Question 451

Symptoms of patent ductus arteriosus

Answer 451

Dyspnoea Failure to thrive Machine like murmur Risk of infective endocarditis

Question 452

Investigations to diagnose patent ductus arteriosus

Answer 452

CXR ECG ECHO

Question 453

Treatment for patent ductus arteriosus

Answer 453

Prostaglandin inhibitor (indomethacin) may induce closure Otherwise consider surgery by catheters

Question 454

What is pulmonary stenosis?

Answer 454

Narrowing of the outflow of the right ventricle can occur in different locations: - Valvar - Sub valvar - Supra valvar - in branches

Question 455

Severe pulmonary stenosis?

Answer 455

-Right ventricular failure as a neonate -Collapse -Poor pulmonary blood flow -RV hypertrophy -Tricuspid regurgitation

Question 456

Moderate/mild pulmonary stenosis?

Answer 456

-well tolerated for many years -right ventricular hypertrophy

Question 457

Treatment of pulmonary stenosis?

Answer 457

Balloon valvuloplasty Open valvotomy Open trans-annular patch Shunt (to bypass blockage)

Question 458

Prevalence of tetralogy of fallot

Answer 458

4-10%

Question 459

What is tetralogy of fallot

Answer 459

Cyanotic! Ventricular septal defect with right ventricular outflow obstruction - therefore O2 deficient blood is systemically shunted = blue blood passes from RV to LV

Question 460

Most common congenital cyanotic heart disease

Answer 460

Tetralogy of Fallot 10% of all congenital birth defects

Question 461

Four congenital abnormalities present in Tetralogy of Fallot

Answer 461

PROV Pulmonary stenosis: RV outflow obstruction Right ventricular hypertrophy Overriding aorta (over top of VSD) Ventricular septal defect (VSD)

Question 462

Symptoms of tetralogy of fallot

Answer 462

Infants are often seen bringing their knees up to their chest as if squatting which partially occluded femoral arteries, this increases systemic vascular resistance and left ventricular pressure => relives cyanosis by reducing right to left shunt *cyanosis often exacerbated when crying or feeding

Question 463

How to diagnose tetralogy of fallot

Answer 463

ECHO CXR - presents as boot shaped heart

Question 464

Treatment of tetralogy of fallot

Answer 464

Full surgical repair within 2y of life and good prognosis if done Normally at 3-6months👩🏻‍🍼

Question 465

Most common congenital heart disease?

Answer 465

Ventricular septal defect 25-30%

Question 466

What is a ventricular septal defect

Answer 466

L->R non cyanotic shunt (not blue) Blood flows from high pressure to low pressure chamber Increased blood flow through the lungs (more in larger defects) Risk of Eisenmengers syndrome and RVH later

Question 467

Symptoms of small ventricular septal defect

Answer 467

Typically asymptomatic Normal heart rate/size Loud systolic murmur

Question 468

Symptoms of a large ventricular septal defect

Answer 468

Exercise intolerance Failure to thrive Murmur varies in instensity Tachycardia + increased respiratory rate Small skinny breathless baby :(

Question 469

Investigation used to diagnose ventricular septal defect?

Answer 469

ECHO

Question 470

Treatment for ventricular septal defect

Answer 470

Spontaneous or surgical closure in infancy if big No need for intervention if small and asymptomatic

Question 471

Eisenmenger’s syndrome?

Answer 471

High pressure pulmonary flow Damages to delicate pulmonary vasculature The resistance to blood flow through lungs increases RV pressure increases Shunt direction reverses Patient becomes BLUE

Question 472

Causes of aortic regurgitation

Answer 472

Congenital bicuspid valve RHD Connective tissue disorders (Marfan/ehlers danos) Infective endocarditis

Question 473

Symptoms and signs of aortic regurgitation

Answer 473

-Collapsing carrigon’s pulse with wide pulse pressure -Quincke’s sign (nailed pulses when pressed) -De Musset sign (head bobbing in time with arterial pulsation)

Question 474

Aortic regurgitation murmur

Answer 474

Early diastolic blowing murmer at right sternal border 2nd intercostal space - Austin fling murmer (severe) - mid diastolic low pitched rumble - heard when regurgitation is so severe blood bounces if mitral valve cusps and makes sound

Question 475

Investigations to diagnose aortic regurgitation

Answer 475

ECG CXR ECHO gold standard, evaluates aortic valve, root, dimensions

Question 476

Treatment for aortic regurgitation

Answer 476

Consider IE prophylaxysis (consider as differential diagnosis) Surgical valve replacement if symptoms

Question 477

What is aortic regurgitation

Answer 477

Leaky aortic valve which makes it insufficient

Question 478

What is aortic stenosis

Answer 478

Pathological narrowing or aortic valve -decrease in flow Normal area 3-4cm Symptoms at 1/4 lumen size Most common valve disorder- results in LV dilation + hypertrophy

Question 479

Symptoms of aortic stenosis

Answer 479

SAD Syncope (exertional) Angina Dyspnoea (relates to heart failure)

Question 480

Aortic stenosis murmur

Answer 480

Ejection systolic crescendo decrescendo, radiating to carotids heard at right sternal border, second IC space -prominent S4 seen in LVH - narrow pulse pressure + slow rising pulse (not collapsing corrigan’s pulse)

Question 481

Investigations to diagnose aortic stenosis

Answer 481

ECG CXR ECHO = gold standard for LV size and function + aortic valve area

Question 482

Treatment for Aortic stenosis

Answer 482

General: Fastidious dental care to prevent IE As it is a mechanical problem-drugs are not effective Surgical if symptomatic: - in a healthy patient -> open repair\valve replaced (definitive) - more at risk (eg 75+) ->TAVI (transcutaneous aortic valve implant) less invasive and stents valve open

Question 483

Differential diagnosis for aortic stenosis

Answer 483

Hypertrophic cardiomyopathy may also cause S4 - associated with sudden death in young men

Question 484

Pathophysiology of aortic stenosis

Answer 484

-A pressure gradient develops between left ventricle and aorta - LV function initially maintained by compensatory pressure hypertrophy - When compensatory mechanism exhausted, LV function declines

Question 485

What does regurgitation cause?

Answer 485

Insufficiency + proximal chamber dilation -loss of structural chamber integrity and strength

Question 486

What does stenosis cause?

Answer 486

Increase in upstream pressure + proximal chamber dilation+hypertrophy - heart becomes huge and rigid; poorly compliant

Question 487

Main valve disorders?

Answer 487

Aortic regurgitation and stenosis Mitral regurgitation and stenosis

Question 488

What do the main valve disorders cause?

Answer 488

Murmers

Question 489

How are murmers best heard?

Answer 489

Using RILE Right side defects (tricuspid /pulmonary) heard on Inspiration Left sided defects (mitral\aortic) heard on Expiration

Question 490

Systolic murmurs?

Answer 490

ASMR Aortic Stenosis Mitral Regurgitation

Question 491

Diastolic Murmer?

Answer 491

ARMS Aortic regurgitation Mitral stenosis

Question 492

Causes of mitral regurgitation

Answer 492

Myxomatous mitral valve (most common valve disease) = mass of cells in valve connective tissue makes leaflets heavier + prolapse

Question 493

What is mitral regurgitation

Answer 493

Heart valve disease in which the valve between the left heart chambers doesn't close completely, allowing blood to leak backward across the valve

Question 494

Risk factors for mitral regurgitation

Answer 494

Females Older Decreased BMI Prior MI Connective tissue disorder (marfan, ehlers danos)

Question 495

Symptoms of mitral regurgitation

Answer 495

Exertion dyspnoea (due to pulmonary hypertension from back logging of blood)

Question 496

Mitral regurgitation murmer?

Answer 496

Pan systolic blowing murmur radiating to axila (at apex) *soft S1, prominent S3 in heart failure (severe cases)*

Question 497

Investigations for diagnosing mitral regurgitation

Answer 497

ECG CXR ECHO (gold standard) - check left atrium size and left ventricle function analysis Also assess valve structure to decide treatment

Question 498

Treatment for mitral regurgitation

Answer 498

ACEi, Bb + serial ECHO monitoring If severe - (symptoms at rest) = valve repair\replacement

Question 499

Normal size of mitral bicuspid lumen and after undergoing stenosis?

Answer 499

Mitral bicuspid lumen = 4-6cm2 Symptoms of stenosis start at <2cm

Question 500

Causes of mitral stenosis

Answer 500

Most common = rheumatic fever (Post strep pyogenes infection) Also valve calcification in older patients + infective endocarditis

Question 501

Pathophysiology of mitral stenosis

Answer 501

RHD (rheumatic heart disease) causes mitral reactive inflammation, after years exacerbated with calcification => LA hypertrophy and chamber dilation

Question 502

Symptoms and signs of mitral stenosis

Answer 502

-malar cheek flush (due to CO2 retention) - association with Atrial Fibrillation (due to stasis in LA and hypertrophy of LA) -dyspnoea - A wave on JVP

Question 503

Mitral stenosis murmur?

Answer 503

Low pitched Mid diastolic murmer Loudest at apex Best heard on expiration with patient lying on left hand side

Question 504

Investigations to diagnose mitral stenosis

Answer 504

CXR (LA enlarged) ECG (AFib, P mitrale= bifid “m” shale P waves when LA enlarged) ECHO -assess valve area, gradient, mobility (gold standard)

Question 505

Treatment for mitral stenosis

Answer 505

Surgical Percutaneous balloon valvotomy (stent open mitral valve opening) Mitral valve replacement

Question 506

Why is mitral stenosis more atrial fibrillation associated?

Answer 506

Mitral stenosis causes left atrium hypertrophy - more chances of embolisation as blood actively pumped harder

Question 507

Risk factors for DVT?

Answer 507

Dependant on Virchow’s triad: 1. Hypercoagulability 2. Venous stasis 3. Endothelial damage (abnormality in any component can result in thrombus)

Question 508

Hypercoagulabilty and causes? (Virchow’s triad)

Answer 508

= increased platelet adhesion and clotting tendency Hereditary: - Factor V Leiden - protein C and S deficiency - antiphospholipid syndrome Acquired: - malignancy - chemotherapy - COCP/HRT - Pregnancy - Obesity

Question 509

Venous stasis and cause? (Virchow’s triad)

Answer 509

=blood flow is normally laminar to spread out platelets and clotting factors without activation Stasis —> aggregation of clotting factors = thrombus formation Cause = immobility (long flights, after surgery)

Question 510

Endothelial damage and causes? (virchow’s triad)

Answer 510

=endothelial cells normally prevent thrombosis by secreting anticoagulants, as well as blocking exposure to pro-thrombotic collagen - damaged endothelial cells cannot!! Causes: — endothelial dysfunction: - smoking — endothelial damage: - surgery - catheter (PICC lines) - Lower limb trauma

Question 511

Symptom and signs of DVT?

Answer 511

Symptom: Unliateral calf pain, redness and swelling Signs: -unliateral swelling -oedema -tender and erythematous -distension of superficial veins

Question 512

What is phlegmasia cerulea dolens?

Answer 512

Occurs in a massive DVT, resulting in obstruction of venous and arterial outflow (rare). => ischemia and a blue, painful leg

Question 513

What is a Wells score?

Answer 513

Calculates the risk of DVT and determines investigations + management >= 2 DVT likely =< 1 DVT unlikely actve cancer, major surgery, calf swelling >3 cm, superficial and tender veins present, pitting oedema in leg, previous dvt.

Question 514

Gold standard for diagnosis of DVT

Answer 514

Duplex ultrasound of leg (Duplex USS) -if unavailable, alternative is D-dimer

Question 515

Flow chart of investigations when considering DVT

Answer 515

wells score likely---> is duplex uss available with 4 hour or not. -yes and DVT = treatment, no and no = no treatment if duplex not available---> D dimer with interim anticoagulation, duplex uss withing 24 hours to see if DVT. unlikley wells---> d dimer if raised then try duplex uss.

Question 516

Positive d-dimer and negative duplex USS? (In patient with suspect DVT)

Answer 516

-stop interim anticoagulation -offer repeat ultrasound 6 to 8 days later +ve= restart anticoagulation -ve= alternative diagnosis

Question 517

Treatment for DVT?

Answer 517

Offer DOACs: apixaban or rivaroxaban If there’s a CI eg patient is renally impaired offer one of: -LMWH -Unfractionated heparin Treatment for at least 3 months or 3 to 6 months if they’re a cancer patient +mobilisation and compression stockings

Question 518

Risk of recurrence with DVT?

Answer 518

30% in the next five years

Question 518

Complications of DVT

Answer 518

Pulmonary embolism Post thrombotic syndrome Increased risk of bleeding (as on anticoagulants)

Question 519

Differential diagnosis to DVT?

Answer 519

Cellulitis Skin infection-typically staph aureus + strep pyogenes -tender, inflamed swollen calf with pronounced demarcation *will show leukocytosis on FBC while DVT will have normal levels*

Question 520

Pathophysiology of types of deep vain thrombosis (DVT)?

Answer 520

Formation of thrombus in a deep leg vein -around\below calf = minor veins (eg. Anterior and posterior tibial) => less concerning and more common -above calf (in thigh) = major veins (eg. Superficial femoral) occlusion may impede distal flow => life threatening and less common

Question 521

Pathophysiology of pulmonary embolism (PE)

Answer 521

Most commonly DVT embolises and lodges in oil on art after circulation (Could be any embolus) Can cause strain on right ventricle due to increased pulmonary vascular resistance

Question 522

What can a PE cause?

Answer 522

PE---> increased pulmomnary vascular resistance---> right ventricular strain ----> cor pulmonale ---> cardiac arrest

Question 523

Risk factors for PE?

Answer 523

Virchow’s triad (Mentioned in detail in DVT)

Question 524

Symptoms of PE

Answer 524

Pleuritic chest pain (present in only 10% of patients) Dyspnoea Cough or haemoptysis Fever Syncope 🚩

Question 525

Signs of PE?

Answer 525

Tachypnoea and tachycardia Hypoxia DVT (swollen tender calf) Pyrexia Hypotension (SBP <90 mmHg suggests massive PE) Elevated JVP (suggest cod Pulmonale)

Question 526

Wells two level score?

Answer 526

Used to determine probability of PE >4: high probability =<4: low probability signs and symptoms, tachycardia, immobilisation etc

Question 527

Process for investigating PE?

Answer 527

D-dimer is NOT diagnostic but CTPA (CT pulmonary angiogram) is -CXR should be normal -ECG: Often find sinus tachycardia S1Q3T3 (classic finding but only in 20% px) RBBB and right axis deviation suggest right heart strain high wells > 4 ---> CTPA and then treat if needed low wells ---> D dimer if raised then CTPA if not then no treatment

Question 528

Why is D-dimer not diagnostic?

Answer 528

Measure of clot burden; a small protein relaxers into blood when blood clot fibronlysed Is sensitive (rules PE in) Not specific (doesn’t rule out other conditions)

Question 529

What’s massive PE?

Answer 529

Hypotensive patient with <90 systolic bp Less common that non massive

Question 530

Treatment for massive PE?

Answer 530

Thrombolysis => alteplase (“clot buster”)

Question 531

Treatment for non massive PE?

Answer 531

Anticoagulation (DOAC) 3 to 6 month treatment 1st line = apixaban\riveroxaban *If there’s a CI due to renal impairment offer LMWH or UFH