Cardiovascular

Question 1

Describe the characteristic, and contrasting, features of chest pain resulting from myocardial ischaemia.

Answer 1

Pain similar to angina (retrosternal, crushing, worse with exertion/cold/after food) but more severe and not relieved by GTN spray.
Associated with nausea, sweating and vomiting.
Patients may experience “angor animi”, a feeling of impending doom.

Question 2

Describe the characteristic, and contrasting, features of chest pain resulting from aortic dissection.

Answer 2

Severe tearing pain, felt behind the shoulder blades. Persistent but worse at onset.
Patient likely to be hypertensive and Marfan-oid.

Question 3

Describe the characteristic, and contrasting, features of chest pain resulting from pleural and respiratory disease.

Answer 3

Sharp pain which is worse on inspiration and coughing. Not central - may be one sided and does not radiate.
May be associated with breathlessness and cyanosis.
Not relieved by GTN spray.

Question 4

Describe the characteristic, and contrasting, features of chest pain resulting from Gastro-oesophageal disease.

Answer 4

GORD presents with ‘heartburn’. Retrosternal burning sensation after food, relieved by antacids.
Oesophageal spasm may be mistaken for MI.
Pain relieved by GTN spray but takes 20 minutes, longer than 2 minute relief present with angina.
Often associated with a history of dysphagia or dyspepsia.

Question 5

Describe the characteristic, and contrasting, features of chest pain resulting from musculoskeletal disease.

Answer 5

Pain localised to one point on the chest
Pain worse on respiring and movement.
Tender to palpation.

Question 6

What is the levine sign?

Answer 6

Levine’s sign is a clenched fist held over the chest to describe ischemic chest pain.

Question 7

Describe the typical history of a patient with ACS.

Answer 7

Severe crushing retrosternal pain of a longer duration than angina pectoris.
This may also be accompanied by autonomic symptoms (these may not be present in elderly patients or those with diabetes.)
Associated symptoms may include: N/V and syncope.
Atypical symptoms include: dyspnoea, plueritic chest pain and indigestion.

Question 8

Describe the clinical features of ACS.

Answer 8

Examination may show systolic murmurs or pulmonary oedema as well as pallor, sweating and tachycardia.
CXR may be normal or show pulmonary oedema or a widened mediastinum (suggesting aortic dissection).
Killip 1 = no crackles and no 3rd heart sound,
Killip 2 = crackles in <50% of lung or 3rd heart sound, Killip 3 = crackles in >50% of lung fields,
Killip 4 = cardiogenic shock.

Question 9

Describe the use of oxygen and analgesia in ACS.

Answer 9

Patients are given high flow oxygen, aspirin, clopidogrel, LMWH.
IV opiates may be administered if necessary, alongside oral/sublingual/IV nitrates.
Anti-emetic must also be administered if opiates used.
Beta-blockers may also be given.

Question 10

Describe the spectrum of the acute coronary syndromes: ST-segment elevation myocardial infarction (STEMI), non-ST-segment elevation syndromes (non-STEMI) and unstable angina (UA).

Answer 10

STEMI:
Complete occlusion of coronary artery.

NSTEMI:
Patients have elevated troponin without ST segment elevation.
Subtotal occlusion of the artery and infarct occurs.

Unstable angina:
Chest discomfort caused by minimal exercise or rest.
Creatine kinase and troponin are normal.
ECG may show ST segment depression or T wave inversion.
Usually atheromatous plaque rupture causes platelet aggregation, lumen narrowing and ischaemia.

Question 11

Describe the role of ECG findings and serum Troponin to establish the diagnosis.

Answer 11

STEMI:
ST segment elevation, elevated troponin.

NSTEMI:
T wave inversion or ST segment depression, troponin elevated. No ST segment elevation.

Unstable angina:
No ECG or troponin changes.

Troponin is released 4-6 hours after the event and peaks at 24 hours. CK-MB (Creatine Kinase Myocardial B fraction) may be a better early marker.
Following ST elevation, R waves decrease in amplitude and Q waves may develop in full thickness infarcts.

Question 12

What is the order of ECG changes following an MI?

Answer 12

First, large peaked T waves (or hyperacute T waves), then ST elevation, then negative T waves and finally pathologic Q waves develop.

Question 13

Describe the role of anti-platelet agents, thrombolysis (including indications and contra-indications), primary percutaneous coronary intervention (PCI) and ‘rescue’ PCI

Answer 13

Anti-platelet agents are first-line therapy in the treatment of occluded coronary vessels.
Fibrinolysis after 12 hours is not supported by evidence, however; if administered before then, it saves 30 lives per 1000 people treated.
Patients who fail to reperfuse after 60-90 minutes (as demonstrated by ECG), may be re-thrombolysed or sent for rescue coronary angioplasty.
PCI is the preferred treatment, within 90 minutes if possible.
PCI can be administered after thrombolysis.
Contraindications to thrombolysis include haemorrhagic stroke (however old), ischaemic stroke (within 6 months), CNS damage, neoplasm and trauma (within 3 months), GI bleed (within last month), any known bleeding disorder or aortic dissection.
Relative contraindications include: Pregnancy, liver damage, refractory hypertension, endocarditis, traumatic CPR, oral anticoagulant therapy.

Question 14

Which anti-platelets are used in ACS?

Answer 14

Aspirin or if allergic clopidogrel.
Ticagrelor in combination with low-dose aspirin is recommended for up to 12 months as a treatment option in adults with acute coronary syndromes (ACS) that is, people:
with ST-segment-elevation myocardial infarction (STEMI)
defined as ST elevation or new left bundle branch block on electrocardiogram.
that cardiologists intend to treat with primary percutaneous coronary intervention (PCI) or
with non-ST-segment-elevation myocardial infarction (NSTEMI).

Question 15

Describe the causes and pathological consequences of ACS.

Answer 15

Atheromatous plaques may fissure, leading to thrombus formation, or bleeding into the plaque.
Complete occlusion of coronary arteries, resulting in ischaemia leads to full thickness ischaemia, unless collateral blood supply is established or lysis occurs.
Such circumferential subendocardial infarction may occur in hypoperfused cardiac tissue, due to stenosed arteries.

Question 16

Describe the difference in prognosis between STEMI, non-STEMI and UA with respect to mortality and morbidity.

Answer 16

6 month mortality in the GRACE registry was 13% for NSTEMI and 8% for UA.
1 month mortality in a community STEMI may be as high as 50%, with 50% of these deaths occurring within 2 hours.
Early death may be due to arrhythmia.
Of those who reach hospital, 80% survive up to 28 days. Prognosis is worse for anterior infarcts than inferior. Morbidity is likely to be related to the level of ischaemia and myocardial damage sustained.

Question 17

Describe the potential complications of ACS: rhythm abnormalities, cardiac failure, ventricular septal defect, ruptured chordae tendineae, haemopericardium, Dressler’s syndrome, ventricular aneurysm and reinfarction.

Answer 17

Rhythm abnormalities (AF, VF, bradyarrhythm),
Cardiac failure (shock),
VSD (Usually occurs in the first week post MI, present with new onset murmur, patients lie flat),
Ruptured chordae tendinae (mitral regurgitation, may present with sudden pulmonary oedema or death),
Haemopericardium (cardiac tamponade),
Dressler’s syndrome (immune mediated pericarditis. Present with frisction rub, chest pain and fever (post-infection/MI)),
Ventricular aneurysm (5-7% of patients following STEMI. Bulging of ventricle, can result in death),
Reinfarction,
Post-infarct angina.

Question 18

Describe the pathway of care developed within the hospital for STEMI/nonSTEMI/UA.

Answer 18

Aspirin 300mg + Clopidogrel 300mg.
Sublingual GTN.
Oxygen (*if <94%, check NICE guideline).
Brief history. IV access and bloods (troponin, FBC, lipids, biochemistry, glucose).
12-lead ECG.
IV opiate and antiemetic.
Beta-blocker if not contraindicated. GPIIb/IIIa inhibitor if PCI available.

“MONA” - Morphine, oxygen, nitrates, aspirin
“BROMANCE” - Beta-blocker, reassurance, oxygen, morphine, aspirin, nitrates, clopidogrel, enoxiparin.

Question 19

What is the TIMI score?

Answer 19

An assessment of morbidity and mortality in MI.
TIMI for STEMI:
age>65,>75, Hx of angina, Hx of hypertension, Hx of DM, systolic BP<100, HR>100, Killip II-IV, weight>67kg, Anterior MI or LBBB, delay to Rx>4hrs.
TIMI for NSTEMI/UA:
age>65, >3 CAD RFs, known CAD (stenosis>50%), aspirin use in last 7 days, severe angina, ST deviation, elevated cardiac markers.

Question 20

What is the GRACE score?

Answer 20

Similar to the TIMI score.

GRACE score is based on age, heart rate, systolic blood pressure, serum creatinine and Killip score.

Question 21

Define stable angina.

Answer 21

Angina is chest discomfort which is precipitated by exercise and relieved with rest.
Usually lasts minutes.
Angina = Strangling.

Question 22

Describe the typical history of a patient with stable angina.

Answer 22

Chest pain relieved by rest.
Pain may be tight, heavy or gripping and is usually located retrosternally but may radiate to the jaw and/or arms.
Cold weather, anger, excitement and food may all provoke angina.
May also cause angor amini, sweating and SOB.

Question 23

Discuss the potential underlying causes of angina 4

Answer 23

Coronary artery disease reduces blood flow to cardiac muscle.
Valvular heart disease puts increased strain on cardiac muscle.
Cardiomyopathy disturbs contractility of cardiac muscle.
Anaemia reduces oxygenation of blood reaching cardiac muscle.

Question 24

Describe relevant clinical features of angina 7

Answer 24

Xanthelasmata - Cholesterol deposits around the eyes, indicating high levels of cholesterol in the blood.
Tendon xanthoma - Appear as slowly enlarging subcutaneous nodules related to the tendons or ligaments. Most commonly found on the hands, feet, and Achilles tendon. Associated with severe hypercholesterolaemia and elevated LDL levels.
HTN
Anaemia
Hyperthyroidism causing tachycardia and irregular rhythm
Aortic stenosis - Ejection systolic murmur heard between heart sounds 1 and 2, may radiate into neck.

Question 25

List recognised risk factors for coronary artery disease. 11

Answer 25

Obesity, smoking, male, hypertension, high cholesterol, hyperlipidaemia, diabetes, low exercise levels, age, family history, type A personality.

Question 26

Describe the pathology of the coronary arteries in patients presenting with angina.

Answer 26

Fatty streaks develop in areas of stress or turbulence. Damage to endothelium causes inflammatory cells to migrate to the area. Macrophages ingest lipid, and release cytokines which stimulate smooth muscle cells to migrate to the intima and lay down hyaline fibrous matter. Macrophages may also release TNF-alpha and IL1 which may lead to the destruction of this fibrous cap and subsequent thrombus formation.

Question 27

Describe the investigation of a patient with suspected angina.

Answer 27

CV examination, resting ECG, FBC, exercise test ECG, scintigraphy, angiography

Question 28

List the classes of drugs used to treat angina, mechanism of action and their common side effects.

Answer 28

Nitrates can relieve angina fairly quickly and are used when required. They cause vasodilation and side effects include headache and hypotension. B-blockers have negative inotropic and chronotropic effects, reducing the strain on the heart. Side effects include fatigue, cold extremities and weight gain. Calcium channel blockers inhibit the excitability of cardiac muscle. Rate limiting blockers such as verapamil and diltiazem inhibit conduction through the AV node and cause a bradycardia, dihydropyridine blockers may reduce contractility but may cause reflex tachycardia so are best used in combination with beta-blockers. Other side effects include dizziness, flushing, headache and peripheral oedema. Nicorandil, a potassium channel agonist, acts similarly to nitrates to reverse angina pain.

Question 29

Use the Framingham/QRISK tools to estimate cardiovascular risk.

Answer 29

The QRISK tools collate risk factor information and estimate a 10 year risk of heart attack or stroke.

Question 30

Outline the ECG changes that may develop during an exercise stress test.

Answer 30

Down sloping ST segment depression, T wave inversion. False positives and false negatives are common (20%), though these patients will have good prognosis.

Question 31

Describe the typical history of pulmonary oedema and its common causes.

Answer 31

SOB, especially when lying down. Paroxsymal nocturnal dyspnoea - patients will wake up in the middle of the night totally out of breath due to fluid shift from interstitium to vascular compartments. Cheynes-stokes respiratory cycles may also occur, due to impaired response of central chemoreceptors to carbon dioxide levels. Common causes include: left sided heart failure, pulmonary hypertension, fluid overload, acute respiratory distress syndrome (causes including: pneumonia, aspiration, sepsis, severe trauma), both acute and chronic kidney disease, hypoalbuminaemia, morphine overdose, tumour, and altitude.

Question 32

Describe the typical clinical features of pulmonary oedema

Answer 32

``` Tachycardia Gallop rhythm - Presence of 3rd heart sound, may be suggestive of stenosis or regurgitation. Bilateral basal crackles Other features may indicate a cause: Raised JVP in heart failure Jaundice in liver failure Hypo or hyper tension ```

Question 33

Discuss the differential diagnosis for pulmonary oedema

Answer 33

If no cardiac cause for pulmonary oedema is present then ARDs should be suspected. Chest infection may produce a cough but is less likely to produce pink frothy sputum and SOB. Pulmonary embolism presents with SOB, pleuritic chest pain and cough.

Question 34

Outline the general principles of management of pulmonary oedema including drugs used in treatment, their route of administration, mechanism of action and their common side effects.

Answer 34

High flow oxygen my be administered to reduce respiratory workload. Obvs, sats and ECG and daily weights must be monitored. Urinary catheter may be inserted and furesemide may be administered, initially IV, then switched to oral. Furosemide is a loop diuretic (blocks Na/K/Cl ion channels in the thick ascending loop of Henle, thus decreasing water reabsorption.) Common side effects include: numbness or tingling, headache, dizziness, blurred vision, low BP, dehydration.

Question 35

Outline the investigations used in acute pulmonary oedema including ECG, CXR, Troponin, and echocardiography.

Answer 35

CXR is used to identify and quantify pulmonary oedema. It will show: Kerly B lines, fluid in the fissures, hazy hila and prominent vasculature (especially superiorly). ECG, troponin and echocardiography will help determine the cause, be it cardiac. FBC, U&Es, LFTs and urine dip are helpful in diagnosis of cause.

Question 36

Define congestive cardiac failure and list common causes.

Answer 36

Congestive heart failure is the failure of both sides of the heart so that not enough blood is pumped out of the heart to adequately perfuse metabolically active tissues. Common causes include ischaemic heart disease (30-35%), cardiomyopathies (30-34%) and hypertension (15-20%). Other causes include: Infection, valvular heart disease, (poor ventricular filling (AV stenosis) or ventricular overload (regurgitation)), congenital heart disease (Septal defect), alcohol and drugs, arrhythmias (AF, tachymyopathy, CHB), pericardial disease and hyperdynamic circulation (anaemia, hyperthyroid, haemochromatosis).

Question 37

Describe the typical history of a patient with CCF.

Answer 37

Exertional dyspnoea Orthopnoea (SOB when lying flat) Fatigue Cachexia (from muscle dissuse, and reduced perfusion)

Question 38

Describe the typical clinical findings in a patient with CCF

Answer 38

Most common clinical findings: RAISED JVP, cachexia, paroxsymal nocturnal dyspnoea, pulmonary oedema, s3 gallop, radiogrpahy cardiomegaly. Less common: Hepatomegaly (causing ASCITES), PERIPHERAL OEDEMA, TACHYCARDIA.

Question 39

What drugs are used to manage CCF?

Answer 39

Diuretcs - reduce water in system, reducing hypertension Beta-blockers - used to reduce contraction force and tachycardia. ACE-i - reduce BP Digoxin Vasodilators

Question 40

Outline the common investigations used to define the cause of CCF.

Answer 40

``` CXR: Cardiomegaly Kerly B wings Bat wings Prominant upper lobe veins Fluid in fissures ``` BNP: Raised in heart failure, if low, HF unlikely. ECG: Indicate cause eg MI, as well as ischaemia, hypertrophy or arrhythmias. Echocardiography: Able to visualise major causes and pathologies such as hypertrophy, valve defects etc.

Question 41

What are the 5 main groups of causes of valvular heart disease?

Answer 41

Congenital (aortic bicuspid) Rheumatic (reaction to group A strep, 50% mitral stenosis) Degenerative Endocarditis (erodes into valves causing insufficiency) Cardiac remodelling

Question 42

What are the congenital causes of valvular heart disease? (4)

Answer 42

Bicuspid aortic valve Lutembacher's syndrome (congenital atrial spetal defect or acquired mitral stenosis) Ebstein Anomaly (tricuspid regurgitation) Fallot’s tetralogy (Pulmonary stenosis)

Question 43

How can degenerative causes lead to valvular heart disease?

Answer 43

Senile calcification of the aortic valve often occurs. | Rupture of chordate tendinae after MI may also occur.

Question 44

How can cardiac remodelling lead to valvular heart disease?

Answer 44

SLE, marfan's, ankylosing spondylitis and syphilis may result in dilation of the valve ring, causing valvular insufficiency.

Question 45

Outline the common symptoms of patients with mitral stenosis or regurgitation (5)

Answer 45

``` If mild, no symptoms Progressive SOB AF Palpitations Cough with frothy sputum Chest infections ```

Question 46

Outline the common symptoms of patients with aortic stenosis or regurgitation (4)

Answer 46

``` Symptoms usually only present when disease is very severe. Exercise induced syncope chest pain SOB Pounding of heart in regurg ```

Question 47

Outline the non-invasive tests used to assess heart valves.

Answer 47

ECG: can show hypertrophies developed due to valvular insufficiencies. Strain patterns due to pressure overload CXR: Can assess for pulmonary hypertension Dilated aorta Calcified valves Echo: Visualise valves and diagnose stenosis. Doppler: Can identify backflow through incompetent valves.

Question 48

What are the signs of mitral stenosis? (5)

Answer 48

``` Malar flush Small volume pulse Raised JVP Thrills/heaves Mid-diastolic rumble murmur ```

Question 49

What are the signs of mitral regurgitation? (5)

Answer 49

``` Pan-systolic murmur Laterally displaced, weak apex beat AF Pulmonary congestion, rs HF Prominent 3rd heart sound ```

Question 50

What are the signs of aortic regurgitation? (9)

Answer 50

``` Bounding or collapsing pulse Quincke’s sign (pulsatile nailbeds), De Musset’s sign (head nodding), Duroziez’s sign (pistol shot femorals), Mueller’s sign (pulsatile uvula), Corrigan’s sign (prominent carotids), Hill’s sign (higher BP in legs), laterally displaced, forceful apex beat high pitched diastolic murmur. ```

Question 51

What are the signs of aortic stenosis? (4)

Answer 51

Small volume, slow rising pulse Forceful apex beat Ejection systolic murmur radiating to carotids (crescendo/decrescendo) Aortic thrills

Question 52

Define infective endocarditis

Answer 52

Infective endocarditis is an endovascular infection of heart valves, endocardium, large intrathoracic vessels and cardiac foreign bodies. Bacteraemia usually has to be associated with endocardium damage.

Question 53

Who is at risk of infective endocarditis? (6)

Answer 53

``` Patients with poor dental hygiene IV drug users Recent dental treatment IV cannulation Recent heart surgery Septal defects ```

Question 54

Describe the typical clinical features of IE. | 3 symptoms, 11 signs

Answer 54

Symptoms: Malaise Pyrexia Arthralgia ``` Signs: Murmurs Splenomegaly Blood in urine petechia Janeways lesions Splinter haemorrhages Oslers nodes Clubbing Roth spots Cerebral emboli Mycotic aneurysm ```

Question 55

List common infecting organisms that cause IE

Answer 55

Mouth - Alpha haemolytic strep viridans IV cannulas, injections - staph aureus Soft tissue infection - streptococcus Gut - Enterococcus

Question 56

Describe the morphological changes seen on an affected heart valve. (2)

Answer 56

Infection usually occurs along the edge of the heart valve, which is also where damage usually occurs. Endocardial damage may allow bacteria to attach, and if incased in a fibrin/platelet mesh, will allow for replication of the bacteria.

Question 57

Describe the pathological complications of infective endocarditis. 4 main consequences

Answer 57

Virulent pyogenic bacteria attach to the leaflets and proliferate. The large crumbly vegetations cause degeneration of valves, chordae and adjacent heart muscle due to spread. This then leads to heart failure. Less virulent bacteria may increase in size gradually to slowly cause HF. Emboli of these collections of bacteria may cause infarction abscesses. Immune complexes from the bacteria may lodge in the glomeruli to cause glomerulonephritis.

Question 58

Outline important investigations for IE 5

Answer 58

Blood cultures should be taken - 3 pairs from different sites. EchoCG - May show evidence of vegetation on valves. FBC - May show normochromic, normocytic anaemia or polymorphonuclear leukocytes. CRP + ESR most likely raised indicating infection. U+Es may show renal dysfunction

Question 59

Outline the general principles of management of suspected and confirmed infective endocarditis.

Answer 59

Antibiotics for 4-6 weeks.

Question 60

Describe the indications for surgery in infective endocarditis. 6

Answer 60

``` Consider surgery if: HF, fungal infection, valvular obstruction, repeated endocarditis, unstable infected prosthetic valve Myocardial abscess. ```

Question 61

Describe how the electrical changes of the cardiac cycle relate to the ECG recording.

Answer 61

P wave = Atrial depolarisation QRS complex = Ventricular depolarisation T wave = Ventricular repolarisation

Question 62

Identify and classify the ECG features of each type of heart block.

Answer 62

1st degree: Prolonged PR interval Mobitz 2nd degree type 1: Progressively prolonged PR interval, until QRS complex is dropped. Mobitz 2nd degree type 2: Regular PR intervals. Some P waves not accompanied by QRS complex. Type 3 - complete HB. No co-ordination between P waves and QRS complexes.

Question 63

Describe the ECG features of atrial fibrillation

Answer 63

Irregularly irregular No P waves present Normal QRS

Question 64

Describe the ECG features of atrial flutter

Answer 64

Saw tooth appearance of P waves | May show 2:1 AV block.

Question 65

Describe the ECG features of re-entrant tachycardia (SVT)

Answer 65

Narrow complex tachycardia | Wolff-Parkinson syndrome = slurred upstroke of QRS complex

Question 66

Describe the ECG features of ventricular tachycardia.

Answer 66

Broad complex tachcardia

Question 67

Describe the ECG features of ventricular fibrillation

Answer 67

No identifiable QRS complexes

Question 68

Describe the ECG features of left and right ventricular hypertrophy

Answer 68

``` LVH: Tall R waves in V5/6 Deep S wave in V1/2 May be some LAD T wave inversion if severe ``` RVH: Deep S wave V6 RAD Peaked P wave and T wave inversion if severe

Question 69

Describe the ECG features of left and right bundle branch block

Answer 69

LBB: WiLLiaM - V1 and V6 RBB: MaRRoW ALTERNATIVELY TURN PAGE 90 DEGREES CLOCKWISE. WHICHEVER WAY QRS COMPLEXES ARE POINTING IS THE SIDE THAT IS BLOCKED.

Question 70

Describe the ECG features of STEMI and the changes over time.

Answer 70

ST elevation. Then Q and T wave inversion begins to develop. Q waves grows larger and larger T waves inverts bigger before receding slightly

Question 71

Identify the common anatomic locations of deep venous thrombosis. 2 areas

Answer 71

Usually veins of legs and pelvis Superficial thrombophlebitis may affect saphenous veins. DVT more commonly affects calf veins. Axillary DVT is very uncommon but can occur.

Question 72

List the risk factors for venous thrombosis. 15

Answer 72

``` Obesity Age Previous DVT/PE Varicose veins Pregnancy Oestrogen therapy Trauma/surgery Venous catheter Cardiorespiratory failure IBD Acute infection Thrombophillia Recent MI Immobility Malignancy ```

Question 73

What is the Wells score and when is it used? 8 criteria

Answer 73

``` Well's score is used to assess risk of DVT. Maximum score of 9, a score of above 1 should raise suspicion of DVT. Criteria: Bedridden >3 days Swollen leg >3cm bigger than other Visible collateral veins localised tenderness in symptomatic leg Malignancy Major surgery Previous DVT Pitting oedema ```

Question 74

Describe the clinical features of a deep venous thrombosis. 6

Answer 74

``` Pain Swelling Redness Engorged superficial veins Oedema Homan's sign (pain on dorsiflexion of the foot) ```

Question 75

Describe the use of a d-dimer test to triage patients with suspected DVT

Answer 75

D-dimers are breakdown products of fibrin. | Clinical diagnosis + raised d dimer has 80% sensitivity

Question 76

Describe a differential diagnosis in patients who present with pain or swelling of the lower limb distinguishing between deep vein thrombosis, superficial thrombo-phlebitis, chronic venous insufficiency, cellulitis, acute arterial ischaemia and hypoproteinaemia

Answer 76

Chronic venous insufficiency = VVV LAPS (Varicose veins, venous ulcers, venous scars, lipodermatosclerosis, atrophy blanche, pitting oedema, scars) Arterial ischaemia = 6 Ps (Pain, pallor, paresthesia, cold, paralysis, pulseless) Cellulitis = 4 signs of infection (redness, swelling, pain, heat) Hypoproteinaemia presents with oedema.

Question 77

Describe the role and range of imaging modalities used when investigating suspected DVT

Answer 77

USS or dopler can be used | Venography with injection of venous contrast is definitive test.

Question 78

Describe the range of clinical presentation and associated pathology of pulmonary embolic disease depending on clot size and cardiopulmonary haemodynamics

Answer 78

Massive - sudden death, large pulmonary hypertension Acute infarction - SOB, pleuritic CP, local tenderness, pleural effusion. Acute, no infarction - tachycardia, tachypnoea, crackels in embulus region, pleuritic CP. multiple emboli - Pulmonary hypertension or cor pulmonale, raised JVP.

Question 79

What is the classification of hypertension based on BP? How many measurements are needed?

Answer 79

<140, <90 = Stage 1 hypertension <160, <100 = Stage 2 hypertension <180, <110 = Stage 3 hypertension At least 3 readings. Should be taken from both arms. Over 14 measurements are used to calculate average when considering ABPM.

Question 80

Describe the clinical and pathological features of 'accelerated phase' or 'malignant' hypertension.

Answer 80

A BP of over 180/120 with signs of papilloedema and/or retinal haemorrhage. Occurs rapidly months-years. Affects people in 3rd or 4th decade. Rapid increase in BP causes fibrinoid necrosis of arterioles: Acute HF, LVH, renal failure, encephalopathuy

Question 81

What are the causes of secondary hypertension?

Answer 81

Renal causes account for 80%: Renal artery stenosis, diabetic nephropathy, chronic GN, polycystic kidney disease, Pregnancy Drugs (NSAIDs, vasopressin, steroids.) Endocrine: Conn's, adrenal hyperplasia, phaeochromcytoma, Cushing's, acromegaly, hyperthyroidism. Congenital: Coarction of the aorta.

Question 82

Describe the pathological consequences of hypertension as they affect the cardiovascular, cerebrovascular and renal systems.

Answer 82

Accelerates atherosclerosis and can cause CAD, PVD, LVH, AAA, dissections Increased risk of strokes Varying levels of nephrosclerosis in kidneys

Question 83

How many Korotkoff sounds are there and what are they?

Answer 83

Sound 1: clear tapping sound (systolic BP) Sound 2: Soft swishing murmur Sound 3: Loud slapping sound Sound 4: Muffling of soun. Sound 5: Disappearance of sound (diastolic BP – depends what book you read).

Question 84

What is the target for cholesterol levels?

Answer 84

Total cholesterol <5mM, LDL <3mM

Question 85

Define atherosclerosis and list the risk factors associated with its development.

Answer 85

Atherosclerosis is an inflammatory condition affecting blood vessels. Fat, macrophages and collagenous material collects on the inside of blood vessels Risk factors: Obesity, smoking, age, HTN, DM, hyperlipidaemia, gender, type A personality, stress, lack of exercise, alcohol.

Question 86

Distinguish between macro- and micro-vascular diseases.

Answer 86

Macrovascular disease may be caused by an MI, stroke, PVD | Microvascular disease occurs in diabetes and is characterised by nephropathy, neuropathy and retinopathy.

Question 87

List specific sites where atheroma may develop.

Answer 87

Usually at branch points, e.g. ostia, bifurcation of the aorta.

Question 88

Describe the common sites and relative incidence of atherosclerotic arterial aneurysms

Answer 88

Usually downward flowing high pressure vessels: Abdominal aorta, iliac vessels, thoracic aorta, popliteal, femoral. Berry aneurysms can occur in Circle of Willis but are not caused by atherosclerosis.

Question 89

Describe the pathophysiology of thoracic aortic dissection

Answer 89

Begins with a tear of the intima. Blood then enters the media. Either re-breaks through intima - double barreled aorta May then break into adventitia - Haemorrhage or backtrack to occlude vessels leaving arch of the aorta or cause haemopericardium. Type A = proximal to the subclavian Type B = Distal to the subclavian

Question 90

What are the symptoms of thoracic aortic dissection?

Answer 90

Tearing pain radiating to back of chest and down arms. Loss of blood supply to CNS may provide accompanying symptoms. Shock. Renal failure Acute limb ischaemia

Question 91

List the symptoms and signs of a ruptured abdominal aortic aneurysm

Answer 91

``` Severe epigastric pain radiating to back Hypotension Tachycardia Anaemia Pulsatile but not expansile mass Grey-Turner's sign (Flank bruising) Cullen's sign (Bruising around umbilicus) ```

Question 92

DDx of AAA

Answer 92

``` Renal colic Diverticulitis Pancreatitis Ruptured peptic ulcer MI ```

Question 93

Describe the role of surveillance monitoring of abdominal aortic aneurysm.

Answer 93

If <5.5cm then ultrasound monitoring is favoured | If over 5.5cm then surgery is favoured

Question 94

List the clinical manifestations of chronic peripheral arterial occlusive disease.

Answer 94

Claudication may cause pain when exercising. Pain in buttocks and thighs, associated with impotence is called Leriche syndrome. Ulcers may be present. ``` Signs: Cold skin Hairless skin Dry skin Buerger's test positive. ```

Question 95

Differentiate symptoms of ischaemic rest pain and neuropathy

Answer 95

Neuropathic pain will not be relieved by swinging legs out of the bed. Neuropathic pain may also be accompanied by allodynia and hyperalgesia.

Question 96

Outline the conservative management of arterial occlusive disease.

Answer 96

Risk factor management: (stop smoking, control BM in DM, resolve HTN, resolve hyperlipidaemia.) Tell them to walk through pain - release VEGF, new vessels grow.

Question 97

Describe the non-invasive and invasive methods for investigation of arterial disease.

Answer 97

ABPI - 0.5-0.95 = intermittent claudication, 0.3-0.5 = pain at rest, <0.3 = Ulceration and gangrene Dopplers USS Angiogram

Question 98

List the causes of acute arterial occlusion.

Answer 98

Either thrombotic (60%) or embolic (30%- trauma, air, iatrogenic, mycotic). Other causes: Trauma, aortic dissection, iatrogenic, popliteal aneurysm

Question 99

Differentiate embolic and thrombotic occlusion.

Answer 99

Thrombotic: Less rapid onest (due to establishment of collateral circulation), more likely to be elderly, artery may feel calcified bruit due to collateral circulation me be present Other leg will have reduced pulses Will have had symptoms in the past ``` Embolic: Sudden onset No prior symptoms Artery will be soft no bruit or collateral circulation Other leg will be fine ```

Question 100

List the symptoms and signs of acute arterial occlusion 6

Answer 100

``` 6 Ps: Pain Paralyses Parasthesia Perishingly cold pulseless Pallor ```

Question 101

Describe the natural history of treated and untreated acute arterial occlusion.

Answer 101

If left untreated, the limb will have to be amputated. Even if treated, reperfusion injury may cause more damage than occlusion via oxidative injury, immflamation. Compartment syndrome may occur. Peripheral nerve damage and chronic pain syndromes.

Question 102

List the underlying diseases or disorders associated with vasospastic changes in the extremities.

Answer 102

Rheumatic autoimmune disorders: SLE, mixed connective tissue disorder, systemic sclerosis and RA. Some haematological conditions: HEP B +C Endocrine disorders such as paraneoplastic syndrome. Neurological causes: Nerve entrapment. Vascular causes: Thrombosis, atherosclerosis Ergot containing drugs, B blockers, oestrogen therapy. May all cause Raynauds syndrome

Question 103

Specify and explain the defining clinical characteristics of Raynaud’s disease (or phenomenon).

Answer 103

``` Spasm of the digital arteries: Pallor Cyanosis Erythema (white, blue, red) Precipitated by the cold More common in females, bilaterally and in hands Attacks may last hours Numbness, burning sensation and severe pain may occur when hands warm up. ```

Question 104

Recognise varicose veins and describe their anatomical distribution.

Answer 104

Dilated, tortuous veins in the lower limb. More common in greater saphenous vein. Dilation of saphenofemoral junction may also occur

Question 105

List the complications of varicose veins.

Answer 105

Haemorrhage into subcutaneous tissue Lipodermatosclerosis (inflammation and pigmentation of gaiter area) Inverted champagne bottle calf Venous ulcers and oedema may also occur as a result of chronic venous insufficiency.

Question 106

Describe the use of the Hand Held Doppler and Duplex-scanning test in diagnosing venous disease

Answer 106

HHD detects the backflow reflux of blood Duplex scanning combines grey-scale USS to visualise vessel architecture and HHD to highlight flow. This can be visualised using colour.

Question 107

Define lymphoedema

Answer 107

An abnormal accumulation of lymph in tissues causing swelling. Mainly in the legs Can create cobblestone effect Most visible on second toe.

Question 108

Outline common causes of lymphoedema.

Answer 108

May be congenital abnormality of lymph vessels - Milroys disease. May be due to a proximal obstruction of lymph vessels via a tumour, inflammation, injury. Surgery to resect lymph nodes. Radiotherapy

Question 109

What are the classic symptoms of asthma 3

Answer 109

Episodic wheeze Cough SOB Are usually reversible and worse in the morning. If poorly controlled may cause wakening at night.