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Cardiovascular > Vascular and Ischaemic Heart Disease > Flashcards

Vascular and Ischaemic Heart Disease Flashcards

1
Q

What is Ischaemia and what does it depend on?

A

Impaired vascular perfusion and it depends on: speed of onset, duration and local demand

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2
Q

What is infarction?

A

Ischaemic necrosis whereby there is a reduction of arterial blood supply or venous drainage

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3
Q

What results in the corruption of haemostats?

A

Thrombosis

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4
Q

What are the two factors involved in haemostasis?

A
  1. maintained blood flow

2. Induce rapid haemostatic plug at site of vascular injury

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5
Q

What is the difference between a thrombus and a blood clot?

A

Thrombus- in life! Has WBC, RBC, platelets, fibrin and lines of Zahn
Blood clot- not in life, no platelets and no lines of Zahn

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6
Q

What are endothelial cells involved in?

A

Regulates inflammation, cell growth, LDL cholesterol

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7
Q

Name the determinants of thrombosis

A

Turbulence and stasis: site and flow

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8
Q

What does impaired venous drainage of the limbs result in?

A

DVT

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9
Q

Name some acquired and genetic prothrombotic factors (hyper coagulation)

A

Acquired: MI, immobilisation, heparin, hyper oestrogen state
Genetic: Factor V mutation, antithrombin III, defects in fibrinolysis

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10
Q

What is the morphology of Thrombi?

A

Occlude lumen–> coronary/femoral/cerebral–> atheroma–> firm attachment to wall–> lines of Zahn

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11
Q

What are lines of Zahn?

A

Layers of solid serum and cells: mural thrombi in LIFE
In ventricles (heart) after MI or arrhythmia
Aortic (aneurysm): atheroma

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12
Q

What are the morphology of venous thrombi?

A

Occlusion–> inflammation–> DVT of calf–> “cast formation of red and blue” (rhubarb and custard)

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13
Q

What are the fates of thrombus?

A

Propigation, embolism, resolution (fibrinolysis), organisation (degranulation)

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14
Q

What are the signs/symptoms of pulmonary infarcts/

A

Wedge shaped, firm, dysponea, chest pain, haemoptysis

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15
Q

What does not cause infarcts in peripheral arterial circulation?

A

Venous emboli

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16
Q

What is Arteriosclerosis and its main targets?

A

Hardening of the arterties (small-medium): aorta, coronary arteries, cerebral arteries

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17
Q

What are the outcomes of Arteriosclerosis?

A

MI, Aortic aneurysm, Peripheral vascular disease, mesenteric artery occlusion, ischamia encephelopathy

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18
Q

What is Atheroscelerosis?

A

A form of arteriosclerosis whereby the composition has:
A lipid core of cholesterol, stress and lipoproteins
Raised focal lesion of intima
Fibrous cap

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19
Q

What is the mechanism of Atheroscelerosis?

A

1) Chronic endothelial injury
2) Endothelial dysfunction
3) Macrophage activation
4) Lipoprotein oxidation
5) Macrophages become foam cells, fatty streak
6) Macrophages die, oxidised lipid stuck in intima= plaque formation

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20
Q

What are the complications of Atheroscelerosis?

A

Ulceration of atheromatous plaque and thrombosis
Haemorrhage into plaque and embolism of plaque contents
On going narrowing- critical stenosis
Aneurysm formation

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21
Q

What are the three components of Virchow’s Triad and which are needed for DVT?

A

Hyper coagulable state, endothelial injury, statin

All three

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22
Q

Name some risk factors for DVT

A

previous DVT, sepsis, nephrotic syndrome, trauma, vasculitis, haemolytic

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23
Q

What does D Dimer testing confirm?

A

It does not specify DVT but if the levels are low it suggests that this is unlikely

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24
Q

What is venous plethysomography?

A

A strain gauge is wrapped around the affected limb and inflated, draining the venous system and the refill time is measured. Can help identify a DVT alongside duplex scanning

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25
Q

What happens if D dimer is positive and Ultrasound is normal?

A

Treat patient and repeat US

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26
Q

What can be used to treat DVT?

A

Anticoagulation with LMWH

Compression stockings which prevent the progression of oedema, thrombosis and phlebitis

27
Q

What is Phlegmasia Dolens?

A

A life threatening extensive thrombotic occlusion which has poor arterial flow into limbs and venous gangrene

28
Q

What is the treatment for Phlegmasia Dolens?

A

and IVC filter to prevent clot from going into the lungs, surgical decompression, only 3-4hrs to fix

29
Q

What is the classifications of acute PTE?

A

Massive with shock of syncope, major with right ventricular dysfunction, major with normal ventricular dysfunction, minor

30
Q

What are some of the classic symptoms of PTE?

A

SOB, collapse, pleuritic chest pain, haemoptysis, sudden death

31
Q

What are some of the signs of PTE?

A

4th heart sound, pleural rub, signs of pleural effusion, consolidation on CXR, wheeze, tachycardia

32
Q

What are the investigations for PTE and the first choice?

A

CTPA is first choice (poor for peripheral), ABG, CXR, VQ perfusion

33
Q

What are you looking for in a echocardiogram in PTE?

A

Right heart strain

34
Q

What is the treatment for a massive PE with shock or syncope?

A

Thrombolysis (streptokinase) or surgery

35
Q

How many days should a patient be on heparin?

A

5 days

36
Q

When are caval filters used?

A

In short term acute, high risk PE

37
Q

What is endarterectomy and when is it used?

A

surgical procedure to remove artheromatous plaque in chronic PE

38
Q

What are the differences between anti platelet, anticoagulation and thrombolytic agents/

A

Antiplatelet: interfere with platelet activity
Anticoagulation: prevents clot formation and extension
Thrombolytic agents: tPA, Strep kinase dissolves existing thrombi

39
Q

What are the clotting factors in Vitamin K?

A

7,9,10,2

40
Q

What does heparin do?

A

Activates antithrombin, inactivates Xa, IXa, XIa

41
Q

What are the durations of therapy for PTE?

A

Temporary risk: 4-6 wks
Idiopathic: 3-6mths
second Idiopathic: lifelong with risk of bleeding

42
Q

When should a patient be coagulated for life?

A

Inherited thrombophilic, antiphospolipid syndrome, recurrent idiopathic VTE, Thromboembolic pulmonary hypertension, recurrent idiopathic VTE

43
Q

What is the definition of intermittent claudification?

A

Muscle ischaemia which is exacerbated through exercise

44
Q

What is the most common site of peripheral vascular disease?

A

Between the thigh and calf

45
Q

What is the liklihood of having an MI with intermittent claudification?

A

More likely than if they’ve had a previous MI

46
Q

What are the non invasive investigations of lower leg ischaemia?

A

Exercise ABPI, Duplex Doppler probe US scanning

47
Q

What are the invasive investigations of lower leg ischaemia?

A

Magnetic Resonance Angiography, CT Angiography, Catheter Angiography

48
Q

What are the treatments of lower leg ischaemia?

A

Stop smoking! Cilostozol (drug), Angioplasty, surgery: Endarterectomy

49
Q

Where is Endarterectomy commonly used?

A

Carotids

50
Q

What is rest pain in critical limb ischaemia?

A

Toe/food ischaemia (worse on sleeping due to decreased CO)

Ulcers/gangrene- severe ischaemia and damage due to trauma or footwear, 10% of diabetics lose feet

51
Q

How can critical limb ischaemia be eased?

A

start on morphine, worse at night, “sitting with leg out of bed”, helped by walking to increase Cardiac output

52
Q

What is the best outcome for amputuation?

A

Below the knee

53
Q

What is the Killip classification?

A

Used in individuals with acute MI to assess them, if they have a low Fillip score, they are less likely to die within the first 30 days of their MI

54
Q

What are the five factors which should be considered when assessing the liklihood of myocardial ischaemia in relation to acute coronary sydromes

A
  1. Nature of the symptoms
  2. History of Ischaemic heart disease
  3. Increasing age
  4. Sex
  5. Number of traditional CV risk factors
55
Q

What are the high risk features of ACS?

A

Prolonged pain (>20mins), worsening angina, pulmonary oedema and arrhythmias

56
Q

What patients should be given a copy of their ECG?

A

Those with bundle branch block or ST segment change

57
Q

Who should be treated with IV Glycoprotein IIb/IIIa receptor antagonists?

A

High risk patients with NSTEMI elevation ACS

58
Q

What should patients with an ST elevation who ACS who do not receive repercussion therapy be treated with?

A

Fondaparinux

59
Q

Who should be considered for beta blockade?

A

Patients with ACS in Killip class I in the absense of bradycardia or hypotension

60
Q

What are the aspirin and clopidogrel guidelines for a patient with NSTEMI?

A

Lifelong aspirin and 3 months clopidogrel

61
Q

What are the aspirin and clopidogrel guidelines for a patient with STEMI?

A

Lifelong aspirin and 4 weeks clopidogrel

62
Q

What treatment should be considered on symptomatic grounds and what monitoring should be done?

A

Amiodarone or sotalol

Monitor the liver and thyroid function every 6 months

63
Q

What are the guidelines concerning rhythm over rate control?

A

Control rate first: if patient is haemodynamically unstable then use electrical cardioversion. If this fails and they are still symptomatic, treat using rhythm control

64
Q

Name a non vitamin K antagonist and a vitamin K antagonist

A

Non: rivaroxaban
K: warfarin

Cardiovascular (8 decks)

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