Diseases Flashcards
What is atherosclerosis?
A progressive disease that is characterised by the build up of plaque within the arteries
What is plaque in the arteries formed from?
Fatty substances, cholesterol, celular waste, calcium and fibrin
What are the two things that can happen to a plaque?
Bleeding into the plaque and formation of a clot on the surface of the plaque
Pathogenesis of atherothrombosis?
Normal -> fatty streak -> Fibrous plaque -> atherosclerotic plaque -> Plaque rupture/ Fissure and thrombosis
What can atherothrombosis cause?
MI, Stroke, Critical leg ischaemia, cardiovascular death
What is ischaemia?
Result of impaired vascular perfusion depriving the affected tissue of nutients
Is ischaemia reversible?
Can be depending on multiple factors including; speed of onset, local demand and duration
What is infarction?
Refers to ischaemic necrosis of a tissue or organ secondary to occlusion/reduction of the arterial supply or venous drainage
What is haemostasis?
Set of well regulated processes that accomplish two important functions;
- maintain blood in a fluid, clot free state in normal vessels
- induce rapid, localised haemostatic plug at site of vascular injury
What is thrombosis?
Formation of a solid or semi-solid mass from the constituents of blood, within the vascular system, during life
Describe thrombogenesis (Virchow’s triad)
Endothelial injury
Hypercoagulability
Changes in blood flow
What is the role of platelets?
Close small breaches in vessel walls
What are the haemostatic contents of platelets?
Alpha granules - adhesion components e.g. fibrinogen, PDGF, anti-heparin etc
Dense granules - ADP
Which molecules to endothelial cells elaborate?
Anticoagulants, antithrombotic, fibrinolytic regulators and prothrombotic molecules
What are the causes of endothelial injury?
Hyperlipidamia, hypertension, smoking, toxins, vasculitis, viruses and immune reactions
What type of flow is blood normally?
Laminar
Which types of blood flow are important in thrombosis?
Turbulence and stasis
What happens when laminar blood flow is disrupted?
Platelets come into contact with the endothelium
Activated clotting factors are not diluted by the normal rapid flow of blood
Inflow of anticoagulant factors is slowed, allowing thrombi to persist
Activation of endothelial cells is promoted
What is hypercoagulability?
Any alteration in the coagulation pathway which predisposes to thrombosis
What are the common sites of arterial thrombi?
Coronary, cerebral and femoral arteries
What are mural thrombi?
Occur on vessel walls
Why are mural thrombi laminated?
There are alternating pale (platelet and fibrin) and dark (RBC/WBC) bands
What is phelbothrobitis?
Inflammation due to venous thrombi
What are the fates of thrombi?
Propagation proximally
Embolisation
Resolution (fibrinolysis)
Organisation
What is an embolism?
Detached intravascular solid, liquid or gaseous mass which is carried by the bloodstream to a site distant from the point of origin
What are thromboemboli?
Fragments of a detached clot
How do pulmonary thromboemboli travel to pulmonary circulation?
Via IVC
What are the exceptions of venous emboli not causing infarcts in peripheral arterial circulation?
Atrial/ventricular septal defect
Paradoxical embolus
When does a fat embolism occur?
Following major soft tissue trauma or major bone fractures
How does a fat embolism cause dyspnoea?
Fatty marrow enters venules, most globules arrest in lungs
How does a fat embolism cause skin rashes/CNS confusion?
Some reach peripheral circulation
When does a gas/air embolism form?
Barotrauma, occurs during delivery or abortion
What is the mechanism of gas/air emboli?
Frothy bubbles occlude major vessels
What is an amniotic fluid embolism?
Amniotic fluid and debris enters torn veins and embolises to lungs
What is a systemic embolism?
An emboli that travels through the systemic arterial ciculation (80% originate from thrombi within heart chambers or on valves
What is arteriosclerosis?
(intimal) Hardening of the arteries
What is Monckeberg medial calcific sclerosis?
Calcification of medium sized arteries in those >50yrs
What is arteriolosclerosis?
Hardening of small arteries and arterioles that’s associated with diabetes mellitus and hypertension
What are the outcomes of atherosclerosis?
Myocardial infarction Peripheral vascular disease Mesenteric artery occlusion Ischaemic encephalopathy (dementia) Aortic aneurysm
In atherosclerosis, as plaque size increase…
Luminal diameter decreases, blood flow reduces, ischaemia results once significant reduction
What are the key stages of atherosclerosis?
- Chronic endothelial injury
- Endothelial dysfunction
- Macrophage activation
- Lipoprotein oxidation
- Foam cell formation
- Plaque formation and growth
Explain endothelial dysfunction
Increased permeability, monocyte adhesion and emigration and platelet adhesion
What are the roles of macrophage activation in atherosclerosis?
- Generation of reactive oxygen species leading to oxidation of lipoproteins
- Production of cytokines which promote chemotaxis and adhesion of further leucocytes
- Production of growth factors contributing to smooth muscle proliferation
How do we resolve atherosclerosis?
Reabsorb lipid at fatty streak stage
High dose statins?
How do we repair atherosclerosis?
Stabilisation by fibrosis
Fish oils?
Calcification
When does intermittent claudication occur?
When insufficient blood reaches exercising muscle
What is claudication?
Muscle ischaemia
What are the non-invasive investigations of lower limb ischaemia?
Measurement of ABPI and duplex US scanning
What are the invasive investigations of lower limb ischaemia?
Magnetic resonance angiography, CT angiography and catheter angiography
What is ABPI?
Ankle pressure divided by brachial pressure
What is a normal ABPI?
0.9 - 1.2
What is the ‘guardian’ therapy of lower limb ischaemia?
- smoking cessation
- Lipid lowering
- Antiplatelets
- Hypertension control
- Diabetes control
- Lifestyle changes
How do you improve claudication symptoms?
Exercise training
Drugs
Angioplasty/stenting
Surgery
Symptoms of critical limb ischaemia?
Pain at rest - requires strong analgesia
Worse pain at night
Helped by sitting and putting leg in a dependent position
Helped by getting up and walking about
Treatment of critical limb ischaemia?
Analgesia
Angiplasty/stenting
Surgical reconstruction/amputation
What is the aetiology of intermittent claudication and critical limb ischaemia?
Smoking, Hypertension, Diabetes, raised cholesterol`
What is the law of LaPlace?
tension = [pressure x radius] / wall thickness
Describe medial degeneration
- Regulation of elastin in aortic wall
- Aneurysmal dilatation
- Increase in aortic wall stress
- Progressive dilatation
What are the risk factors for an AAA?
Male, FHx, Age, Smoking, CV disease, cerebrovascular disease, hypertension, hypercholesterolaemia, diabetes
What are the signs and symptoms off a ruptured/non ruptured AAA?
Pain (abdominal, back, ? renal colic), collapse, ‘trashing’
Potential signs and symptoms of a ruptured an AAA?
May not look well, tachycardic, hypotensive, pulsatile (expansile mass +/- tender), transmitted pulse, peripheral pulses
What are the investigations of an AAA?
US scan, CT scan
How can a CT scan help in an AAA?
Shows us shape, size and illiac involvement
Allows for management planning
What is an elective aneurysm repair?
Prophylactic operation to reduce risk of rupture balanced against risk of procedure
What is an emergency aneurysm repair?
Therapeutic operation balancing expectation of death against the risk of the procedure
Describe EVAR (Endovascular Aneurysm repair)
- Exclude AAA from ‘inside’ the vessel
- inserted via a peripheral artery
- X-ray guided
- Modular components
Describe the open repair of an AAA
Laparotomy, clamp aorta and iliacs, dacron graft, tube vs bifurcated graft
What do you need to get blood out of the legs?
A vessel
Valves
A pump
What are the two venous systems in the legs?
Deep system (tibials, popliteal and femoral) Superficial system (saphenous and perforators )
What are varicose veins?
Dilated, tortuous superficial veins, due to transmission of deep vein pressure
What is vital in the diagnosis of chronic venous disease?
Past medical history
Why do you get varicose veins following a DVT?
Conditions that can increase the deep veins pressure:
- Deep vein obstruction
- Deep valve incompetence
What are the signs of varicose veins?
Dilated and tortuous superficial veins
More prominent with standing
Arising in groin or behind the knee
What are some of the potential complications of varicose veins?
- Bleeding and bruising
- Superficial thrombophlebitis
- Chronic venous insufficiency
What is thrombophlebitis?
Inflammation of a vein caused by a blood clot:
- sore
- significant
- scarring
What is chronic venous insufficiency?
irreversible skin damage as a result of sustained ambulatory venous pressure
What is chronic venous ulceration?
Break in the skin between malleoli and tibial tuberosity
What are the investigations of chronic venous diseases?
Duplex scan (colour doppler)
What is the non-interventional management of chronic venous disease?
Information Graduated compression ( 4 layer bandages and stockings)
When is non-interventional management of chronic venous disease contraindicated?
In patients with a low ABPI
What is the interventional management of chronic venous disease?
Surgical (high tie, stripping or foam, mutiple stab avulsions)
Endovenous (duplex guided)
Foam sclerotherapy
What is a stroke?
Acute onset of focal neurological symptoms and signs due to disruption of blood supply
What are the two types of strokes?
Haemorrhagic and ischaemic
Explain a haemorrhagic stroke
Raised BP
Weakened blood vessel wall due to:
- structural abnormalities
- inflamm of vessel wall (vasculitis)
What are the non-modifiable risk factors for a stroke?
Age FHx Gender Race Previous stroke
What are the modifiable risk factors for a stroke?
Hypertension Hyperlipidaemia Smoking Diabetes AF Obesity
What conditions does a stroke mimic?
Hypoglycaemia Seizure Migraine Other metabolic conditions Space occupying lesions in the brain
What is the only way of differentiating between an ischaemic and haemorrhagic stroke?
Brain imaging
- CT brain
- MRI with DWI
- MRI with GRE - looks for old haemosiderin deposits
What is the medical management of a stroke?
Aspirin 75mg and Clopidogrel 75mg daily
Statins
Antihypertensives - more important in stroke than in CHD
What is the surgical management of a stroke?
Haemotoma evacuation
Relief of raised intracranial pressure
Carotid endarterectomy
Five things for cardiology clinical diagnosis?
History, physical signs, ECG, non-invasive investigations and invasive investigations
What are the classical clinical signs/symptoms in valvular heart disease?
Chest pain (on exertion), SOB, syncope
What are the features of classic cardiac SOB?
Related to activity
Often associated with peripheral oedema
Orthopnoea
Paroxysmal Nocturnal Dyspnoea (PND)
4 types of breathless classifications ?
Class I, II, III and IV
Based on patient’s limitation
5 things to remember in clinical cardiology exam?
General appearance, Arterial pulse, venous pulse (JVP), palpation (Apex beat, heaves and thrills), auscultation (heart sounds and murmurs)
What is an innocent murmur?
A murmur that is not of any pathological significance
Where are innocent murmurs?
They are always localised to the pulmonary area - if it’s not in the pulmonary area then it isn’t an innocent murmur
What are the three causes of aortic stenosis?
Congenitally bicuspid valve (has 2 cusps instead of 3)
Age related/degenerative
Rheumatic
What are the clinical features of aortic stenosis?
SOB, chest pain, Syncope on exertion
Low volume pulse
Forceful apex - LV heave
Ejection systolic murmur, maximal in the aortic area that radiates to the carotids