Cardiovascular conditions 2 Flashcards

2nd half of cardiovascular conditions Valve and vascular conditions

1
Q

What is aortic regurgitation?

A

Reflux of blood from the aorta into the left ventricle during diastole, due to a weakened aortic valve. Also known as aortic insufficiency

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2
Q

What causes aortic regurgitation?

A

Abnormal backflow of blood leads to pathological changes - left ventricular chamber enlargement and hypertrophy takes place to maintain a normal CO

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3
Q

What are the Risk factors for aortic regurgitation?

A

Aortic valve leaflet abnormalities or damage

  • Bicuspid aortic valve
  • Infective endocarditis
  • Rheumatic fever
  • Trauma
  • Age

Aortic root/ascending aorta dilatation

  • Systemic hypertension
  • Aortic dissection
  • Aortitis
  • Arthritides (e.g. RA, seronegative arthritides)
  • Connective tissue disease (Marfan’s, Ehler-danlos)
  • Pseudoxanthoma elasticum, osteogenesis imperfecta
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4
Q

What are the symptoms for aortic regurgitation?

A

Chronic
- Initially asymptomatic
- Late symptoms of heart failue (e.g. exertional dyspnoea, orthopnoea, fatigue)
- Palpitations, angina and syncope, CCF
Acute
- Sudden cardiovascular collapse (left ventricle cannot adapt to rapid increase in end-diastolic volume)

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5
Q

What are the signs of aortic regurgitation?

A

Collapsing pulse
Wide pulse pressure
Thrusting and heaving displaced apex beat
Early diastolic murmur over the aortic valve region (heard best when sitting forward with breath help at top of expiration)
An ejection systolic murmur may also be heard due to increased flow across the valve

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6
Q

What Eponymous signs are seen in Aortic regurgitation?

A
  • Austin-flint mid-diastolic murmur (Heard over apex)
  • Quincke’s sign (pulsation on nail bed)
  • De Musset’s sign (Head nodding with pulse)
  • Becker’s sign (pupil and retinal artery pulsation)
  • Muller’s sign (Pulsation of uvula)
  • Corrigan’s sign (Pulsation in neck)
  • Traube’s sign (Pistol shot [loud systolic and diastolic sounds] on auscultation of femoral arteries)
  • Durozies’s sign (systolic and diastolic bruit heard on partial compression of femoral artery)
  • Rosenbach’s sign (systolic pulsations of liver)
  • Gerhard’s sign (Systolic pulsation of the spleen)
  • Hill’s sign (Popliteal cuff systolic pressure exceeding brachial pressure >60)
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7
Q

What are the investigations for Aortic regurgitation?

A

CXR (Cardiomegaly, dilatation of ascending aorta, signs of pulmonary oedema)
ECG (LVH)
Echocardiogram (show underlying cause, or effects of aortic regurgitation, doppler echo)
Cardiac catheterisation with angiography (functional state of ventricles or the presence of coronary artery disease) - helps assess severity of lesion, aortic root anatomy, LV function

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8
Q

How can you see left ventricular hypertrophy on ECG?

A

Deep S in V1/2
Tall R in V5/6
Inverted T waves in Lead I, aVL, V5/6
Left axis deviation

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9
Q

What is Aortic stenosis?

A

Narrowing of the left ventricular outflow at the level of the aortic valve?

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10
Q

What causes aortic stenosis?

A

Stenosis can be secondary to Rheumatic heart disease (most common worldwide)
Congenital: Calcification of a congenital bicuspid aortic valve, william’s syndrome
Calcification/degradation of a tricuspid aortic valve in the elderly (Senile calcification)

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11
Q

What are the risk factors for Aortic stenosis?

A

Age > 60

CKD

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12
Q

What are the symptoms of aortic stenosis?

A

May be asymptomatic initially
Aortic stenosis in elderly patients with chest pain, exertional dyspnoea or syncope
Angina (due to an increased Oxygen demand of the hypertrophied left ventricle)
Syncope or dizziness on exercise
Symptoms of heart failure

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13
Q

What are the signs of Aortic stenosis?

A

Narrow pulse pressure with slow-rising pulse
Heaving, undisplaced apex beat
Ejection systolic murmur at the aortic area, radiation to the carotid artery
Second heart sound may be softened or absent
A bicuspid valve may produce an eejiton click

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14
Q

What are the investigations for aortic stenosis?

A

ECG
- P mitrale
- LVH
- LBBB or complete AV block
CXR
- Post-stenotic enlargement of ascending aorta
- Calcification of aortic valve
- LVH
Echocardiogram (diagnostic)
- visualises structural changes of the valves and level of stenosis (valvar, supravalvar or subvalvar)
- Estimation of aortic valve area and pressure gradient across the valve in systole
- Assess left ventricular function
Doppler echo can estimate gradient across valves

Severe stenosis if gradient >/= 50mmHg and valve area <1cm^2
If aortic jet velocity >4ms risk of complications is increased

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15
Q

What is Mitral regurgitation?

A

Retrograde flow of blood from left ventricle to left atrium during systole due to mitral valve insufficiency

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16
Q

What are the causes of mitral regurgitation?

A

Caused by mitral valve damage or dysfunction, which in turn could be caused by any of the following:

  • Rheumatic heart disease
  • Infective endocarditis
  • Mitral valve prolapse
  • Papillary muscle rupture or dysfunction (Secondary to IHD or cardiomyopathy)
  • Chordal rupture and floppy mitral valve associated with connective tissue disease
  • Functional: LV dilatation
  • Annular calcificaiton
  • Congenital
  • Cardiomyopathy
  • Appetite suppressants (fenfluramine)
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17
Q

What are the symptoms for Mitral regurgitation?

A

Acute MR - May present with symptoms of LVF
Chronic MR - asymptomatic or present with:
- Exertional dyspnoea
- Palpitations if in AF
- Fatigue
Mitral valve prolapse - asymptomatic or atypical chest pain or palpitations

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18
Q

What are the signs of mitral regurgitation?

A
Pulse may be irregularly irregular (AF)
Laterally displaced apex beat with thrusting
Pansystolic murmur
- Loudest apex beat
- Radiates to axilla
- Soft S1
- S3 may be heard due to rapid ventricular filling
Signs of LVF in acute
Mitral valve prolapse
- Mid-systolic click
- Late systolic murmur
- The click moves towards S1 when standing and away when laying down
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19
Q

What investigations are done for Mitral regurgitation?

A

ECG (Normal, may show AF or P mitrale)
CXR
- Acute MR shows signs of LVF
- Chronic (Left atrial enlargement, cardiomegaly, mitral valve calcification, pulmonary oedema)
Echo (Perform 6-12 months)
Doppler Echo
Cardiac catheterisation to confirm diagnosis, exclude other valve disease, assess CAD

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20
Q

What is Mitral Stenosis?

A

Mitral valve narrowing causes obstruction to blood flow from the left atrium to the left ventricle

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21
Q

What causes Mitral stenosis?

A
Mainly: Rheumatic heart disease
Rarer causes:
- Congenital mitral stenosis
- Mucopolysaccharidoses
- Endocardial fibroelastosis
- Prosthetic valve
- SLE
- Rheumatoid arthritis
- Endocarditis
- Atrial myxoma
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22
Q

What are the symptoms of Mitral stenosis?

A
Fatigue
Exertional dyspnoea
Chest pain
Orthopnoea
Palpitations (related to AF)
Systemic emboli
Rarer symptoms (chronic bronchitis type picture)
- Cough
-Haemoptysis
- Hoarseness caused by compression of left recurrent laryngeal nerve by an enlarged left atrium
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23
Q

What are the signs of Mitral stenosis?

A

Peripheral cyanosis
Malar flush (decreased CO)
Irregularly irregular pulse
Low volume pulse
Apex beat in right place and tapping
Parasternal heave (RV hypertrophy, secondary to pulmonary hypertension)
Loud S1 with opening snap
Mid-diastolic murmur heard best in expiration with patient laying on their left
Graham steel murmur may occur
Evidence of pulmonary oedema on lung auscultation

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24
Q

What are the investigations for mitral stenosis?

A

ECG
- Normal
- May see P mitrale
- May see AF - Evidence of RVH if severe pulmonary hypertension)
CXR
- Left atrial enlargement [double shadow in Right cardiac sillhouette]
- cardiac enlargemen
- pulmonary congestion/oedema
- Mitral valve calcification [occurs in rheumatic cases])
Echocardiography
- Assess functional and structural impairments
- Transoesophageal echocardiogram (TOE) gives a better view
Cardiac catheterisation
- Measure severity of heart failure

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25
Q

What is tricuspid regurgitation?

A

Backflow of blood from the right ventricle to the right atrium during systole

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26
Q

What causes tricuspid regurgitation?

A

Congenital
- Ebstein’s anomaly
- Cleft valve in ostium primum
Functional
- Consequence of Right ventricular dilatation (e.g. due to pulmonary hypertension)
- Valve prolapse
Rheumatic heart disease
Infective endocarditis (IV drug user)
Other: Carcinoid syndrome, traume, cirrhosis, iatrogenic
Drugs e.g. Ergot-derived dopamine agonists i.e. bromocriptine, cabergoline, pergolide

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27
Q

What are the risk factors for Tricuspid regurgitation?

A
Right ventricular dilatation from pulmonary hypertension for left heart failure
Rheumatic heart disease
Infective endocarditis
Carcinoid syndrome
Permanent pacemaker
Congenital
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28
Q

What are the symptoms of Tricuspid regurgitation?

A
Fatigue
Breathlessness
Palpitations
Headaches
Nausea
Anorexia
Epigastric pain made worse by exercise
Jaundice 
Lower limb swelling
Ascites 
Oedema
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29
Q

What are the signs of tricuspid regurgitation?

A
Irregularly irregular pulse
Raised JVP (Giant V waves)
Palpation
Auscultation
- Pansystolic murmur
- Louder on inspiration (Carvallo sign)
- Loud P2 component of second heart sound
Chest exam:
- Pleural effusion
- Cases of pulmonary HTN
Abdominal exam:
- Palpable liver 
- Ascites
- Jaundice
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30
Q

What investigations are done for Tricuspid regurgitation?

A
FBC
LFT
Cardiac enzymes
Blood culture
ECG 
- P pulmonale [R atrial hypertrophy]
Echo
- Extent of regurgitation can be estimated using doppler US
- May show valve prolapse and RV dilation
Right heart catheterisation
- Rarely  needed
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31
Q

What is aortic dissection?

A

A condition where a tear in the aortc intima allows blood to surge in the aortic wall, causing a split between inner and outer tunica media, creating a false lumen.

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32
Q

How do you classify aortic dissection?

A
Type A:
Ascending aorta (most common - 70%)
Type B:
Descending aorta (distal to left subclavian artery - 30%)
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33
Q

What causes aortic dissection?

A

Preceded by degenerative changes in the smooth muscle of aortic media
Expansion of false lumen leads to obstruction of branches of the aorta: Subclavian, carotid, coeliac and renal arteries
- Hypoperfusion of target organs give rise to symptoms
- Unequal arm pulses and BP
- Anterior spinal artery (acute limb ischaemia, paraplegia)
- Renal arteries (anuria)
- If moves proximally, develop aortic valve incompetence, inferior MI and cardiac arrest

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34
Q

What are the risk factors for aortic dissection?

A
Hypertension
Aortic atherosclerosis
Connective tissue disease (e.g. Marfan's, Ehlers-Danlos, SLE)
Congenital cardiac abnormalities (coarctation of the aorta)
Aortitis
Iatrogenic
Trauma 
Crack cocaine
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35
Q

What are the symptoms of Aortic dissection?

A
Main symptom: Sudden central 'tearing' pain, may radiate to the back in between shoulder blades (can mimic MI)
Other symptoms caused by obstruction of branches of aorta:
- Hemiparesis, dysphasia, black out
- Chest pain
- Ataxia, loss of consciousness
- Paraplegia
- Severe abdo pain
- Anuria, Renal failure
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36
Q

What are the signs of aortic dissection?

A
Murmur on back (below left scapula)
Hypertension
Blood pressure difference between 2 arms
Wide pulse pressure
Hypotension suggests tamponade
- Check for pulsus paradoxus
- Include: Tamponade, pericarditis, chronic sleep apnoea, obstructive lung disease
Signs of aortic regurgitation (high volume collapsing pulse, early diastolic murmur over aortic area)
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37
Q

What are the investigations of aortic dissectoin?

A
FBC
Cross-match 10 units of blood
U&amp;Es (check renal function)
Clotting screen
CXR (Widened mediastinum)
ECG ( Maybe signs of LVH and inferior MI)
Echo (TOE allows visualisation)
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38
Q

What is an Abdominal Aortic Aneurysm?

A

A localised enlargement of the abdominal aorta such that the diameter is >3cm or >50% larger than normal diameter.
A true aneurysm is an abnormal dilatation involving all layers of the arterial wall
- Can be fusiform [most] or sac-like

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39
Q

What is a pseudo aneurysm?

A

False aneurysms involving a collection of blood in the outer layer only (adventitia) which communicates with the lumen e.g. after trauma

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40
Q

What causes an AAA?

A

No specific causes
Unruptured aneurysms occur due to degeneration of elastic lamellae and smooth muscle loss
Ruptured AAAs leak into the retroperitoneal space (relatively stable) or intraperitoneal space (results in shock)

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41
Q

What are the Risk Factors for AAA?

A

Severe atherosclerotic damage to aortic wall
Family history
Smoking
Male
Age
Hypertension
Hyperlipidaemia
Connective tissue disorders (marfan’s, Ehlers-Danlos)
Inflammatory disorders (Behcets, Takayasu arteritis)

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42
Q

What are the symptoms of AAA?

A
Unruptured
- No symptoms
- Incidental finding
- May have pain in back, abdomen, loin or groin
Ruptured
- Pain in abdomen - intermittent or continuous
- Pain may be sudden or severe
- Syncope - low bp
- Shock
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43
Q

What are the signs of AAA?

A

Pulsatile and laterally expansile mass on bimanual palpitation of the abdominal aorta
Abdominal bruit
Retroperitoneal haemorrhage (Can cause Grey-turner’s)
Hypotension
Tachycardia

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44
Q

What are the investigations for AAA?

A
FBC
Clotting screen
Renal function
Liver function
Cross-match
Doppler US
CT with contrast
MRI angiography
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45
Q

At what size AAA is needed for management?

A

Women - 5cm

Men - 5.5cm

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46
Q

What are Arterial ulcers?

A

A localised are of drainage and breakdown of skin due to inadequate arterial blood supply.
Usually seen on feet of patients with severe atheromatous narrowing of the arteries supplying the legs

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47
Q

What causes arterial ulcers?

A

Ulcers are caused by a lack of blood flow to the capillary beds of the lower extremities

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48
Q

What are the risk factors for arterial ulcers?

A
Coronary heart disease
History of stroke or TIA
Diabetes mellitus
Peripheral artery disease (e.g. intermittent claudication, critical limb ischaemia)
Obesity and immobility
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49
Q

What are the symptoms of arterial ulcers?

A

Often distal (Dorsum of foot or between toes)
Punched-out appearance
Often elliptical with clearly defined edges
Ulcer base contains grey, granulation tissue
Night pain - hallmark of arterial ulcers (worse when supine, relieved by dangling leg off end of bed)

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50
Q

What are the signs of arterial ulcers?

A
Night pain
Punched out appearance
Hairlessness
Pale skin
Absent pulses
Nail dystrophy
Wasting of calf muscles
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51
Q

What investigations are done for arterial ulcers?

A

Duplex ultrasonography of lower limbs - assess patency of arteries and potential for revascularisation or bypass surgery
ABPI
Percutaneous angiography
ECG
Fasting serum lipids, fasting blood glucose and HbA1c (diabetes is major RF)
FBC (anaemia can worsen ischaemia)

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52
Q

What is DVT?

A

Formation of thrombus within deep veins (most commonly in calf or thigh)

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53
Q

What causes DVT?

A

Deep veins in the legs are more prone to blood stasis hence clots are more likely to form
Virchow’s triad

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54
Q

What is Virchow’s triad?

A

Stasis of blood flow
Endothelial injury
Hypercoagulability

55
Q

What are the Risk factors for DVT?

A
Medical hospitalisation in last 2 months
Major surgery within 3 months
Lower-extremity trauma
Severe trauma
Factor V lieden 
Smoking
Obesity
Family history
Use of specific drugs (Contraceptive pill, tamoxifen, thalidomide)
Increasing age
Medical comorbidity
56
Q

What are the symptoms of DVT?

A

Swollen limb
May be painless
Mild fever

57
Q

What are the signs of DVT?

A
Local erythema, warmth and swelling, tenderness
Difference in leg circumference
Varicosities (Swollen/tortuous vessels)
Skin colour changes
Homan's sign
Pitting oedema
Mild fever
Risk stratified using Well's criteria
58
Q

What is Homan’s sign?

A

Forced passive dorsiflexion of the ankle causes deep calf pain

59
Q

What is Well’s score?

A
Active cancer
Bedridden >3 days or major surgery in last 12 weeks
Calf swelling >3cm
Collateral veins present
Entire leg swollen
Localised tenderness along the DVT
Pitting oedema
Paralysis, paresis 
Previously documented DVT
Alternative diagnosis as likely or morye likel
60
Q

What are the investigations for DVT?

A
Well's score (if <2 - D-dimer)
- If normal excluded
- If raised do duplex USS
If pregnant do duplex USS straight away
INR and aPTT
Urea and Creatinine
LFTs
FBC
if PE suspected (ECG, CXR, ABG)
61
Q

How do you manage DVT?

A

Anticoagulation
Offer LMWH or Fondaparinux
- Severe renal impairment / CKD stage 4/5 offer unfractionated heparin (UFH) with dose adjustments
- Increased risk of bleeding consider UFH
LMWH those with active cancer and confirmed proximal DVT or PE
Oral anticoagulant with confirmed DVT or PE - traditionally warfarin, now NOACs (rivaroxaban, dabigatran and apixaban)
Below-knee stockings manages symptoms
Inferior vena cava filters to those with DVT or PE and no anticoagulation available
Look for thrombophilia in those with no cause under 40
Over 40, think of cancer

62
Q

What are the complications of DVT?

A
Pulmonary embolism
Bleeding during initial treatment
Heparin-induced thrombocytopenia
Heparin resistance/aPTT confounding
Post-thrombotic syndrome
Bleeding during long-term/extended term
Osteoporosis due to heparin treatment
63
Q

What is post-thrombotic syndrome?

A

20-40% of those with DVT
Presents with pain, swelling, hyperpigmentation, dermatitis, ulcers, gangrene and lipodermatosclerosis

Risks: Older age, obesity, history of previous ipsilateral DVT
Low risk in asymptomatic DVT

64
Q

What is dyslipidaemia?

A

Hypercholesterolaemia
Raised total cholesterol and/or low-density lipoprotein cholesterol or non-high density lipoprotein cholesterol in the blood.

65
Q

What causes dyslipidaemia?

A

Lipid travels in blood packaged with proteins as lipoproteins
4 classes: Chylomicrons, VLDL, LDL, HDL

66
Q

What are the types of dyslipidaemia?

A

Those with Raised high-LDL: Familal primary hyperlipidaemia, secondary: Cushing’s, hypothyroidism, nephrotic syndrome or cholestasis.

Mixed hyperlipidaemia: Both LDL and TG high, due to T2DM, metabolic syndrome, alcohol abuse, chronic renal failure

67
Q

What are the risk factors for Dyslipidaemia?

A
Insulin resistance and type 2 diabetes mellitus
Excess body weight (BMI>25)
Hypothyroidism
Cholestatic liver disease
Cigarette smoking
Nephrotic syndrome
Use of certain medications
68
Q

Which medications cause dyslipidaemia?

A
Thiazide diuretics
Oral Oestrogen
Glucocorticoids
Anabolic steroids
Atypical antipsychotics such as: Olanzapine
69
Q

What are the symptoms for Dyslipidaemia?

A

No own symptoms but does lead to symptomatic vascular disease such as: CAD, stroke and PVD

70
Q

What are the signs for dyslipidaemia?

A
Corneal arcus
Xanthomas
Metacarpophalangeal joints
Xanthelasma
Familial hypercholesterolaemia
Milky white appearance of retina
71
Q

What are the investigations for dyslipidaemia?

A

Lipid profiles
Serum TSH
Lipoprotein (>50mg/dL)

72
Q

What is the management for dyslipidaemia?

A

Lifestyle advice (BMI 20-25; Diet of <10% calories from fats, Exercise)
Treatments differ for familial or secondary hyperlipidaemia
Medications
- 1st: Simvastatin
- 2nd: Fibrates e.g. Bezafibrate or cholesterol absorption inhibitors e.g. ezetimibe
(Hypertriglyceridaemia responds best to fibrates, nicotinic acid or fish oil)

73
Q

What are the treatment priorities for dyslipidaemia?

A

Using statins in primary prevention
1st: All those with known CVD
2nd: All with DM
3rd: Those with 10 years risk of CVD >20%
Aim for target plasma cholesterol of less than or equal to 4

74
Q

What are the complications for dyslipidaemia?

A
Ischaemic heart disease
Periphreral vascular disease 
Acute coronary syndrome
Stroke
Erectile dysfunction
75
Q

What is Gangrene?

A

Gangrene tissue necrosis, either wet with superimposed infection, dry or gas gangrene (due to poor vascular supply)

76
Q

What is dry gangrene?

A

Necrosis without infection

77
Q

What is wet gangrene?

A

Tissue death and infection

78
Q

What is gas gangrene?

A

Subset of necrotising myositis caused by spore-forming clostridial species

79
Q

What causes gangrene?

A

Tissue ischaemia and infarction
Physical trauma
Thermal injury
Gas gangrene is caused by clostridia perfringens

80
Q

What are the risk factors for Gangrene?

A
Diabetes
Peripheral vascular disease
Atherosclerosis
Smoking/alcohol
Renal disease
Leg ulcers
Malignancy
Immunosuppression
Steroid use
Puncture/surgical wounds
Trauma
81
Q

What are the symptoms of gangrene?

A

Pain
Discolouration of affected area (black)
Often affects extremities of areas subject to high pressure
Gas gangrene: Rapid onset of myonecrosis, muscle swelling, gas production, sepsis, severe pain

82
Q

What are the signs of gangrene?

A

Painful area - erythematous region around gangrenous tissue
Gangrenous tissue - Black due to haemoglobin break down products
Wet gangrene - Tissue becomes boggy with pus and smelly caused by active anaerobes
Gas gangrene - spreading infection and destruction of tissues causes overlying oedema, discolouration and crepitus

83
Q

What are the investigations for gangrene?

A
FBC
U&amp;Es
Glucose
CRP 
Blood culture
Wound swab
Pus/fluid aspirate
Xray of affected area - may see gas gangrene
84
Q

What is Hypertension?

A

Systolic pressure >140mmHg and/or diastolic >90mmHg on 3 seperate occasions

85
Q

What is malignant hypertension?

A

> 200/>130 mmHg

86
Q

What causes hypertension?

A
Disturbance of auto-regulation
Excess sodium intake
Renal sodium retention
Dysregulation of the RAS axis with elevated plasma renin activity
Increased sympathetic drive
Increased peripheral resistance
Endothelial dysfunction
Cell membrane transport perbutations
Insulin resistance/hyperinsulinaemia
87
Q

What are secondary causes of Hypertension?

A
Renal artery stenosis
Chronic glomerulonephritis
Chronic pyelonephritis
PKD
Chronic renal failure
Renovascular disease
Diabetes mellitus
Hyperthyroidism
Cushing's syndrome
Conn's syndrome
Hyperparathyroidism
Phaeochromocytoma
CAH
Acromegaly
Coarctation of the aorta
Increased intravascular volume
Sympathomimetics
Corticosteroids
COCP
Pre-eclampsia
Isolated systolic hypertension (due to stiffening of large arteries)
Malignant (Rapid rise in BP leading vascular damage, usually severe HTN + B/L retinal haemorrhages
88
Q

What are the risk factors for Hypertension?

A
Obesity
Aerobic exercise <3 times a week
Moderate/high alcohol intake
Metabolic syndrome
Diabetes mellitus
Black ancestry
Age >60 years
Family history of HTN or CAD
Sleep apnoea
Sodium intake >1.5g/day
Low fruit and vegetable intake
Dyslipidaemia
89
Q

What are the symptoms of hypertension?

A
Often asymptomatic
Symptoms of complications
Symptoms of cause 
Accelerated or malignant hypertensiton
- Scotomas (visual field loss)
- Blurred vision
- Headache
- Seizures
- Nausea and vomiting
- Acute heart failure
90
Q

What are the signs of hypertension?

A

Blood pressure measured 2/3 times
Examination reveals information on the causes:
- Radiofemoral delay
- Renal artery bruit
- Palpable kidneys
- Signs of phaeochromocytoma or Cushing’s
- End organ damage (LVH, Retinopathy, proteinuria)
- S4 and heave

91
Q

How is hypertensive retinopathy classified?

A

Using Keith-Wagner classification

  • Grade I: Silver wiring
  • Grade II: Silver wiring + AV nipping
  • Grade III: Flame haemorrhage, sometimes cotton wool spots
  • Grade IV: Papilloedema
92
Q

What are the investigations for hypertension?

A
U&amp;Es
Glucose
Lipids
Check Renin, aldosterone and 24hr urine for catecholamine
Exclude secondary causes
Dipstick (Bloods and protein)
Ambulatory BP monitoring
Others if secondary cause suspected:
- Renal angiography
- Urinary free cortisol
- Renin
- Aldosterone
- MR aorta
93
Q

What is the management of Hypertensoin?

A

Conservative management

  • Stop smoking
  • Lose weight
  • Reduced alcohol intake
  • Reduced dietary sodium

Medicines.

94
Q

What is the medicines used for hypertension (140-159/90-99)?

A

Black patients or >55:

  • CCB or thiazide
  • Then add ACEi or ARB or combine thiazide and CCB
  • Then CCB + Thiazide + ACEi/ARB

Non-black patients:

  • ACEI/ARB
  • Then add CCB or thiazide
  • Then CCB + Thiazide + ACEi/ARB

If still needed: Spironolactone, Beta blockers

95
Q

What medicines are used if their BP >160/100?

A

All patients start with 2 drugs

  • CCB / Thiazide + ACEi / ARB
  • If needed: CCB + Thiazide + ACEi
96
Q

What is the target BP you are aiming for?

A

<80: 135/85

80

97
Q

What is used for severe hypertension management?

A

Atenolol and Nifedipine

98
Q

How do you manage acute malignant hypertension?

A

IV beta blocker
Labetolol
Hydralazine sodium nitropusside

99
Q

What is the problem with rapidly lowering BP?

A

Causes cerebral infarction

100
Q

What are the comlpications for hypertension?

A
Coronary artery disease
Cerebrovascular accident
Left ventricular hypertrophy
Congestive heart failure
Retinopathy
Peripheral artery disease
Chronic kidney disease
Aortic dissection
Malignant hypertension
101
Q

What is Peripheral vascular disease?

A

Occurs due to atherosclerosis causing stenosis of arteries via a multifactorial process involving modifiable and non-modifiable risk factors

102
Q

What causes peripheral vascular disease?

A

Atherosclerosis in peripheral arteries
Intermittent claudication and ciritcal limb ischaemia, seperate to acute limb ischaemia.
Leads to tissue loss (Gangrene/ulceration)

103
Q

What are the risk factors for peripheral vascular disease?

A
Smoking
Diabetes
Hypertension
Hyperlipidaemia
Physical inactivity
Obesity
Family history
Renal failure
104
Q

What are the symptoms of peripheral vascular disease?

A

Intermittent claudication

105
Q

Which vein is affected in calf claudication and buttock claudication?

A

Calf claudication = Femoral disease

Buttock claudication = Iliac disease

106
Q

What are the signs of peripheral vascular disease?

A
Acute limb ischaemia 
- Pain
- Pale
- Pulseless
- Paralysis
- Paraesthesia
- Perishingly cold
Others:
- Atrophic skin
- Hairless
- Punched-out ulcers (often painful)
- Colour change when raising leg (Buerger's angle)
107
Q

What investigations are done for peripheral vascular disease?

A
History + Vascular exam 
First line: ABPI
- Normal is 1-1.2
- Peripheral arterial disease is 0.5-0.9
- Critical limb ischaemia is <0.5
- Tissue loss is <0.2
THEN colour duplex ultrasoun
- Non-invasive
- shows stenosis
GOLD STANDARD: MRI/CT ANGIOGRAM
Blood pressure
FBC
Fasting glucose
Lipid levels
ECG
Thrombophilia screen
U&amp;E
108
Q

What is Pulmonary hypertension?

A

An increase in mean pulmonary arterial pressure which can be caused by or associated with a wide variety of other conditions

109
Q

What causes pulmonary hypertension?

A
  • Idiopathic
  • Left ventricular failure
  • Lung disease
  • Thromboses/Emboli in lungs
110
Q

What are the risk factors for pulmonary hypertension?

A

Obesity
Family history of pulmonary hypertension
Cocaine use
Predisposing diseases (COPD/Interstitial lung disease/Fibrosis)

111
Q

What are the symptoms for pulmonary hypertension?

A
Progressive breathlessness
Weakness/tiredness
Exertional dizziness and syncope
Angina and tachyarrhythmias
Late stage - oedema and ascites
112
Q

What are the signs of pulmonary hypertension?

A
Right ventricular heave
Loud pulmonary second heart sound
Murmur (Pulmonary regurgitation)
Tricuspid regurgitation
Raised JVP
Peripheral oedema
Ascites
113
Q

What are the investigations for pulmonary hypertension?

A
CXR (exclude lung disease)
ECG - RVH and strain
Pulmonary function tests
LFTs 
Lung biopsy - interstitial lung disease
Echocardiography - assess right ventricular function
Right heart catheterisation
114
Q

What are varicose veins?

A

Varicose veins are subcutaneous, permanently dilated veins 3 mm or more in diameter when measured in a standing position

115
Q

What are the causes of varicose veins?

A

Venous valve incompetence is most common aetiology
Blood pools left when valves don’t function properly, leading to increased pressure and distention of the veins
Primary causes:
- Genetic or developmental weakness in vessel walls.
- Results in increased elasticity, dilatation and valvular incompetence
- Congenital valve absence.
Secondary causes:
- Pregnancy
- DVT
- Ovarian tumours
- Pelvic malignancy
- Ovarian cysts
- Ascites
- Lymphadenopathy
- Retroperitoneal fibrosis

116
Q

What are the risk factors for varicose veins?

A
Increasing age
Family history
Female sex
Increasing number of births
DVT
Occupation with prolonged standing
Obesity
117
Q

What are the symptoms of varicose veins?

A
Complaining about cosmetic appearance
Aching/cramps in the legs
Aching worse at end of day
Swelling
Tingling
Heaviness and restless legs
Itching
Bleeding
Infection
Ulceration
118
Q

What are the signs of Varicose veins?

A
  • Inspect when standing
  • Oedema, eczema, phlebitis, atrophies’ blanche, lipodermatosclerosis
  • Trendelenburg test (allow localisation of sites of valvular incompetence)
  • Signs of venous insufficiency (Varicose eczema, haemosiderin staining, atrophie blanche, lipodermatosclerosis, oedema, ulceration)
119
Q

What are the investigations for varicose veins?

A

Duplex ultrasound - assess for reversed flow, roughly, valve closure time >0.5 seconds indicates reflux while valve closure time >1 second

120
Q

What is the management for varicose veins?

A

Symptomatic superficial vein insufficiency
- 1st line: Graduated compression stockings
- If ineffective: Phlebotomy or sclerotherapy
- If effective: Ablative procedures +/- phlebotomy or sclerotherapy
For Deep vein insufficiency (Phlebotomy and compression stockings)

121
Q

What are the management types for DVT?

A

Conservative
Endovascular treatment
Surgery

122
Q

What are the conservative management for DVT?

A

Exercise - improves skeletal muscle pump
Elevation of legs at rest
Support stiockings

123
Q

What are the endovascular treatments for DVT?

A

Radiofrequency ablation: Catheter inserted into vein and heated
Endovenous laser ablation
Injection sclerotherapy
Phlebectomy

124
Q

What are the Surgical treatments for DVT?

A

Saphenofemoral ligation
Stripping of the long saphenous vein (groin to upper calf)
Avulsion of the varicosities
Post op: Bandage legs tightly and elevate for 24 hours

125
Q

What are the complications for varicose veins?

A
Chronic venous insufficiency
Haemorrhage
Venous ulceration
Lipodermatosclerosis
Haemosiderin deposition
DVT
Pulmonary embolus
Paraesthesia from injury to sural nerve
126
Q

What are venous ulcers?

A

Large, shallow, sometimes painful ulcers usually found superior to the medial malleoli.
They are caused by incompetent valves in the lower limbs leading the venous stasis

127
Q

What causes venous ulcers?

A

Associated with varicose veins, varicose enzymes, haemosiderin pigmentation, atrophie blanche and venous flare
Oedema of lower leg present and chronic venous stasis lead to warty hyperplasia
Caused by incompetent valves in the veins of the lower leg, especially in perforaters. Causes blood to be squeezed out into superficial veins, when calf muscles are contracted, instead of upwards to the heart.
Dilation of superficial veins occurs (varicosities) and the subsequent raised venous pressure resulting in oedema, venous eczema and ulceraton

128
Q

What are the risk factors for venous ulcers?

A
Obesity
Immobility
Recurrent DVT
Varicose veins 
Previous injury / surgery to the leg
Age
129
Q

What are the symptoms of venous ulcers?

A

Large, shallow, relatively painless ulcer with an irregular margin above the medial malleoli

130
Q

What are the signs of venous ulcers?

A

Stasis eczema
Lipodermatosclerosis
Haemosiderin deposition

131
Q

What are the investigations of venous ulcers?

A

ABPI (<0.8)
Measure surface area of ulcer
Swab for microbiology
Biopsy (if possibly mahorlin’s ulcer)

132
Q

What is Majorlin’s ulcer?

A

Aggressive squamous cell carcinoma, presenting in an area of previously traumatized, chronically inflamed , or scarred skin

133
Q

How do you manage venous ulcers?

A

Graduated compression (reduced venous stasis)
Debridement and cleaning
Antibiotics (if infected)
Topical steroids

134
Q

What are the complications of venous ulcers?

A

Recurrence

Infection