Diseases Flashcards

1
Q

What is atherosclerosis?

A

A progressive disease that is characterised by the build up of plaque within the arteries

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2
Q

What is plaque in the arteries formed from?

A

Fatty substances, cholesterol, celular waste, calcium and fibrin

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3
Q

What are the two things that can happen to a plaque?

A

Bleeding into the plaque and formation of a clot on the surface of the plaque

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4
Q

Pathogenesis of atherothrombosis?

A

Normal -> fatty streak -> Fibrous plaque -> atherosclerotic plaque -> Plaque rupture/ Fissure and thrombosis

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5
Q

What can atherothrombosis cause?

A

MI, Stroke, Critical leg ischaemia, cardiovascular death

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6
Q

What is ischaemia?

A

Result of impaired vascular perfusion depriving the affected tissue of nutients

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7
Q

Is ischaemia reversible?

A

Can be depending on multiple factors including; speed of onset, local demand and duration

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8
Q

What is infarction?

A

Refers to ischaemic necrosis of a tissue or organ secondary to occlusion/reduction of the arterial supply or venous drainage

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9
Q

What is haemostasis?

A

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
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10
Q

What is thrombosis?

A

Formation of a solid or semi-solid mass from the constituents of blood, within the vascular system, during life

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11
Q

Describe thrombogenesis (Virchow’s triad)

A

Endothelial injury
Hypercoagulability
Changes in blood flow

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12
Q

What is the role of platelets?

A

Close small breaches in vessel walls

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13
Q

What are the haemostatic contents of platelets?

A

Alpha granules - adhesion components e.g. fibrinogen, PDGF, anti-heparin etc
Dense granules - ADP

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14
Q

Which molecules to endothelial cells elaborate?

A

Anticoagulants, antithrombotic, fibrinolytic regulators and prothrombotic molecules

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15
Q

What are the causes of endothelial injury?

A

Hyperlipidamia, hypertension, smoking, toxins, vasculitis, viruses and immune reactions

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16
Q

What type of flow is blood normally?

A

Laminar

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17
Q

Which types of blood flow are important in thrombosis?

A

Turbulence and stasis

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18
Q

What happens when laminar blood flow is disrupted?

A

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

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19
Q

What is hypercoagulability?

A

Any alteration in the coagulation pathway which predisposes to thrombosis

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20
Q

What are the common sites of arterial thrombi?

A

Coronary, cerebral and femoral arteries

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21
Q

What are mural thrombi?

A

Occur on vessel walls

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22
Q

Why are mural thrombi laminated?

A

There are alternating pale (platelet and fibrin) and dark (RBC/WBC) bands

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23
Q

What is phelbothrobitis?

A

Inflammation due to venous thrombi

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24
Q

What are the fates of thrombi?

A

Propagation proximally
Embolisation
Resolution (fibrinolysis)
Organisation

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25
Q

What is an embolism?

A

Detached intravascular solid, liquid or gaseous mass which is carried by the bloodstream to a site distant from the point of origin

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26
Q

What are thromboemboli?

A

Fragments of a detached clot

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27
Q

How do pulmonary thromboemboli travel to pulmonary circulation?

A

Via IVC

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28
Q

What are the exceptions of venous emboli not causing infarcts in peripheral arterial circulation?

A

Atrial/ventricular septal defect

Paradoxical embolus

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29
Q

When does a fat embolism occur?

A

Following major soft tissue trauma or major bone fractures

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30
Q

How does a fat embolism cause dyspnoea?

A

Fatty marrow enters venules, most globules arrest in lungs

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31
Q

How does a fat embolism cause skin rashes/CNS confusion?

A

Some reach peripheral circulation

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32
Q

When does a gas/air embolism form?

A

Barotrauma, occurs during delivery or abortion

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33
Q

What is the mechanism of gas/air emboli?

A

Frothy bubbles occlude major vessels

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34
Q

What is an amniotic fluid embolism?

A

Amniotic fluid and debris enters torn veins and embolises to lungs

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35
Q

What is a systemic embolism?

A

An emboli that travels through the systemic arterial ciculation (80% originate from thrombi within heart chambers or on valves

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36
Q

What is arteriosclerosis?

A

(intimal) Hardening of the arteries

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37
Q

What is Monckeberg medial calcific sclerosis?

A

Calcification of medium sized arteries in those >50yrs

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38
Q

What is arteriolosclerosis?

A

Hardening of small arteries and arterioles that’s associated with diabetes mellitus and hypertension

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39
Q

What are the outcomes of atherosclerosis?

A
Myocardial infarction 
Peripheral vascular disease
Mesenteric artery occlusion 
Ischaemic encephalopathy (dementia) 
Aortic aneurysm
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40
Q

In atherosclerosis, as plaque size increase…

A

Luminal diameter decreases, blood flow reduces, ischaemia results once significant reduction

41
Q

What are the key stages of atherosclerosis?

A
  • Chronic endothelial injury
  • Endothelial dysfunction
  • Macrophage activation
  • Lipoprotein oxidation
  • Foam cell formation
  • Plaque formation and growth
42
Q

Explain endothelial dysfunction

A

Increased permeability, monocyte adhesion and emigration and platelet adhesion

43
Q

What are the roles of macrophage activation in atherosclerosis?

A
  • 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
44
Q

How do we resolve atherosclerosis?

A

Reabsorb lipid at fatty streak stage

High dose statins?

45
Q

How do we repair atherosclerosis?

A

Stabilisation by fibrosis
Fish oils?
Calcification

46
Q

When does intermittent claudication occur?

A

When insufficient blood reaches exercising muscle

47
Q

What is claudication?

A

Muscle ischaemia

48
Q

What are the non-invasive investigations of lower limb ischaemia?

A

Measurement of ABPI and duplex US scanning

49
Q

What are the invasive investigations of lower limb ischaemia?

A

Magnetic resonance angiography, CT angiography and catheter angiography

50
Q

What is ABPI?

A

Ankle pressure divided by brachial pressure

51
Q

What is a normal ABPI?

52
Q

What is the ‘guardian’ therapy of lower limb ischaemia?

A
  • smoking cessation
  • Lipid lowering
  • Antiplatelets
  • Hypertension control
  • Diabetes control
  • Lifestyle changes
53
Q

How do you improve claudication symptoms?

A

Exercise training
Drugs
Angioplasty/stenting
Surgery

54
Q

Symptoms of critical limb ischaemia?

A

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

55
Q

Treatment of critical limb ischaemia?

A

Analgesia
Angiplasty/stenting
Surgical reconstruction/amputation

56
Q

What is the aetiology of intermittent claudication and critical limb ischaemia?

A

Smoking, Hypertension, Diabetes, raised cholesterol`

57
Q

What is the law of LaPlace?

A

tension = [pressure x radius] / wall thickness

58
Q

Describe medial degeneration

A
  • Regulation of elastin in aortic wall
  • Aneurysmal dilatation
  • Increase in aortic wall stress
  • Progressive dilatation
59
Q

What are the risk factors for an AAA?

A

Male, FHx, Age, Smoking, CV disease, cerebrovascular disease, hypertension, hypercholesterolaemia, diabetes

60
Q

What are the signs and symptoms off a ruptured/non ruptured AAA?

A

Pain (abdominal, back, ? renal colic), collapse, ‘trashing’

61
Q

Potential signs and symptoms of a ruptured an AAA?

A

May not look well, tachycardic, hypotensive, pulsatile (expansile mass +/- tender), transmitted pulse, peripheral pulses

62
Q

What are the investigations of an AAA?

A

US scan, CT scan

63
Q

How can a CT scan help in an AAA?

A

Shows us shape, size and illiac involvement

Allows for management planning

64
Q

What is an elective aneurysm repair?

A

Prophylactic operation to reduce risk of rupture balanced against risk of procedure

65
Q

What is an emergency aneurysm repair?

A

Therapeutic operation balancing expectation of death against the risk of the procedure

66
Q

Describe EVAR (Endovascular Aneurysm repair)

A
  • Exclude AAA from ‘inside’ the vessel
  • inserted via a peripheral artery
  • X-ray guided
  • Modular components
67
Q

Describe the open repair of an AAA

A

Laparotomy, clamp aorta and iliacs, dacron graft, tube vs bifurcated graft

68
Q

What do you need to get blood out of the legs?

A

A vessel
Valves
A pump

69
Q

What are the two venous systems in the legs?

A
Deep system (tibials, popliteal and femoral) 
Superficial system (saphenous and perforators )
70
Q

What are varicose veins?

A

Dilated, tortuous superficial veins, due to transmission of deep vein pressure

71
Q

What is vital in the diagnosis of chronic venous disease?

A

Past medical history

72
Q

Why do you get varicose veins following a DVT?

A

Conditions that can increase the deep veins pressure:

  • Deep vein obstruction
  • Deep valve incompetence
73
Q

What are the signs of varicose veins?

A

Dilated and tortuous superficial veins
More prominent with standing
Arising in groin or behind the knee

74
Q

What are some of the potential complications of varicose veins?

A
  • Bleeding and bruising
  • Superficial thrombophlebitis
  • Chronic venous insufficiency
75
Q

What is thrombophlebitis?

A

Inflammation of a vein caused by a blood clot:

  • sore
  • significant
  • scarring
76
Q

What is chronic venous insufficiency?

A

irreversible skin damage as a result of sustained ambulatory venous pressure

77
Q

What is chronic venous ulceration?

A

Break in the skin between malleoli and tibial tuberosity

78
Q

What are the investigations of chronic venous diseases?

A

Duplex scan (colour doppler)

79
Q

What is the non-interventional management of chronic venous disease?

A
Information 
Graduated compression ( 4 layer bandages and stockings)
80
Q

When is non-interventional management of chronic venous disease contraindicated?

A

In patients with a low ABPI

81
Q

What is the interventional management of chronic venous disease?

A

Surgical (high tie, stripping or foam, mutiple stab avulsions)
Endovenous (duplex guided)
Foam sclerotherapy

82
Q

What is a stroke?

A

Acute onset of focal neurological symptoms and signs due to disruption of blood supply

83
Q

What are the two types of strokes?

A

Haemorrhagic and ischaemic

84
Q

Explain a haemorrhagic stroke

A

Raised BP
Weakened blood vessel wall due to:
- structural abnormalities
- inflamm of vessel wall (vasculitis)

85
Q

What are the non-modifiable risk factors for a stroke?

A
Age
FHx
Gender 
Race
Previous stroke
86
Q

What are the modifiable risk factors for a stroke?

A
Hypertension 
Hyperlipidaemia 
Smoking 
Diabetes 
AF 
Obesity
87
Q

What conditions does a stroke mimic?

A
Hypoglycaemia 
Seizure 
Migraine 
Other metabolic conditions 
Space occupying lesions in the brain
88
Q

What is the only way of differentiating between an ischaemic and haemorrhagic stroke?

A

Brain imaging

  • CT brain
  • MRI with DWI
  • MRI with GRE - looks for old haemosiderin deposits
89
Q

What is the medical management of a stroke?

A

Aspirin 75mg and Clopidogrel 75mg daily
Statins
Antihypertensives - more important in stroke than in CHD

90
Q

What is the surgical management of a stroke?

A

Haemotoma evacuation
Relief of raised intracranial pressure
Carotid endarterectomy

91
Q

Five things for cardiology clinical diagnosis?

A

History, physical signs, ECG, non-invasive investigations and invasive investigations

92
Q

What are the classical clinical signs/symptoms in valvular heart disease?

A

Chest pain (on exertion), SOB, syncope

93
Q

What are the features of classic cardiac SOB?

A

Related to activity
Often associated with peripheral oedema
Orthopnoea
Paroxysmal Nocturnal Dyspnoea (PND)

94
Q

4 types of breathless classifications ?

A

Class I, II, III and IV

Based on patient’s limitation

95
Q

5 things to remember in clinical cardiology exam?

A

General appearance, Arterial pulse, venous pulse (JVP), palpation (Apex beat, heaves and thrills), auscultation (heart sounds and murmurs)

96
Q

What is an innocent murmur?

A

A murmur that is not of any pathological significance

97
Q

Where are innocent murmurs?

A

They are always localised to the pulmonary area - if it’s not in the pulmonary area then it isn’t an innocent murmur

98
Q

What are the three causes of aortic stenosis?

A

Congenitally bicuspid valve (has 2 cusps instead of 3)
Age related/degenerative
Rheumatic

99
Q

What are the clinical features of aortic stenosis?

A

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