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Supporting Life > Vascular Diseases > Flashcards

Vascular Diseases Flashcards

1
Q

What is the normal thickness of the left ventricular wall

A

14mm

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2
Q

What is the normal thickness of the right ventricular wall

A

Less than 4mm

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3
Q

What does white in heart muscle represent

A

Necrotic tissue

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4
Q

What is arteriosclerosis

A

Group of disorders that have in common thickening and loss of elasticity of arterial walls

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5
Q

What is atherosclerosis

A

Progressive disease affecting the intima (affects the lumen) of elastic and muscular arteries characterised by focal atheromas (fibrofatty plaques) consisting of a lipid core covered by a fibrous cap.

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6
Q

What is Monckeberg’s medial scloeriss

A

Calcification of media (composed of smooth muscle cells) of muscular arteries

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7
Q

What is arteriolosclerosis

A

Proliferative or hyalien thickening of the walls of small arteries and arterioles

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8
Q

What are RF for atherosclerosis

A

diet and hyperlipidaemias, hypertension (systolic and diastolic), smoking, DM

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9
Q

What is T1 of atheromatous plaque

A

Lipid is present in the macrophages in the intima (can go between gaps in adjacent endothleium cells or use lipoprotein receptors - process of transcytosis)

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10
Q

What is T2 of atheromatous plaque

A

Smooth muscle cell i addition to macrophages. Smooth muscle cells can migrate into intima from underlying media. In the intima, smooth muscle cells start phagocytosing lipid and start synthesising collagen

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11
Q

What is T3 of atheromatous plaque

A

Lesions in the aorta

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12
Q

What is T4 of atheromatous plaque

A

Complex plaque (stains with Elastic van Gieson - collagen is red). Plaque causes underlying muscle to atrophy. Arterial wall becomes weaker. Can get abnormal swelling of the wall. The intima and inner 2/3rd of the media is usually oxygen and nutrients by diffusion from blood in the lumen of the artery. Oxygen and nutrients cannot diffuse through plaque.

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13
Q

What is the sequence of atherogenesis

A

Atheromas are occlusive, compromising blood flow to distal tissues and causing ischaemic injury. Most problems occur in coronary arteries

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14
Q

What happens after the rupture of a fibrous cap of the plaque

A

Sub endothelium collagen is exposed and lipids to coagulation factors in the blood. Thrombosis can then develop on top of plaque. Can precipitate sudden change in coronary flow -> NSTEMI or STEMI

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15
Q

What is thrombosis

A

Complication of late stage atherosclerosis. Organisation of thrombi may contribute to plaque formation and luminal encroachment. Fibirin can usually be detected

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16
Q

How does endothelial injury contribute to atherogenesis

A

Increased expression of vascualr cell adhesion molecules ICAM-1 and VCAM-1 increases monocyte adhesion

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17
Q

What are the effects of atherosclerosis

A

Slow, insidious narrowing of the vascular lumina, resulting ischaemia of the tissues perfused by the involved vessels - seen as intermittent claudication in the legs
Sudden occulsion of the lumen by superimposed thrombosis or haemorrhage into an atheroma, producing ischaemia

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18
Q

What is the P wave

A

Atrial depolarisation

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19
Q

What is the QRS complex

A

Ventricular depolarisation

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20
Q

What is Q

A

Intraventricular septum depolarisation

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21
Q

What is R

A

Main mass depolarisation

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22
Q

What is S

A

Base depolarisation

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23
Q

What is ST

A

Period of zero potential between ventricular depolarisation and repolarisation

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24
Q

What is the T wave

A

Ventricular repolarisation

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25
Q

How is MI diagnosed

A

Troponin T and I - T binds to tropomyosin, interlocking them to form troponin-tropomyosin complex. and I binds to actin in thin myofilaments to hold the troponin-tropomyosin complex in palce

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26
Q

What does cardiac I and T indicate

A

Myocardium damage

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27
Q

How do cardiac muscles contract

A

Calcium induced calcium release mechanisms. Ca2+ enters L type calcium channels. Ca22+ detected by ryanodine receptors, causing a positive feedback response. Ca2+ binds to troponin C, moving the tropomyosin complex off the acting binding site, allowing the myosin head to bind to the actin filament

28
Q

Why is chest pain felt

A

Ischaemia->metabolites accumulate in the interstitium of heart muscle->adenosine accumulation so ATP isn’t recharged->activate nerve endings

29
Q

What causes angina

A

Plaque can restrict blood flow to cause stable angina. When stenosis reaches 70%, blood flow can no longer reach demand

30
Q

What are the sensations of MI

A

Site and radiation (diffuse, anterior chest, left arm, neck)
Character (tight, pressure, weight, constriction, dull)
Triggers (exercise, cold, meals, psychological stress)
Relief (rest, GTN0

31
Q

What is the duration of MI sensation

A

Less than 30 minutes is angina, over 30 minutes is infarction

32
Q

What causes STEMI

A

Epicardial coronary artery blockage

33
Q

What happens when an atherosclerotic plaque ruptures

A

Platelets initiate clotting cascade. Fibrinogen is polymerising to form fibrin, trapping RBCS

34
Q

What does statin do

A

Lower’s cholesterol

35
Q

Why does SOB occur with MI

A

Starling’s law of the heart -> left ventricular end-diastolic pressure needs to increase -> left atria pressure increase -> Starling’s law of capillary flow -> increase in hydrostatic pressure pushes fluid out of capillaries into the interstitium of the lungs -> pO2 drops more than pCO2 goes up

36
Q

What are the advantages of mechanical reperfusion

A

Faster
Less stroke and bleeds
Lower mortality
High % reperfusion

37
Q

What is the difference between STEMI and NSTEMI

A

Reperfusion therapy necessary for STEMI as it indicates a completely blocked artery. In NSTEMI, blood flow is limited by stenosis.

38
Q

What is a T1 MI

A

Spontaneous MI (plaque rupture, ulceration, erosion or dissection)

39
Q

What is a T2 MI

A

MI secondary to ischaemic imbalance (endothelial dysfunction, spasm, coronary embolism, tach/brady arrhythmia, anemia, hypoxia, hypotension)

40
Q

What is a T3 MI

A

MI causing death before biomarkers available

41
Q

What is the assessment steps for suspected MI

A

Start therapy before troponin results
Measure cardiac troponin in all px with symptoms of ACS
Measure serial cardiac troponin I or T at 3-6 hours after symptom onset
Use risk scores to assess prognosis

42
Q

What are anti-anginal drugs

A 
Beta-adrenoreceptor blockers
L type calcium channel blockers
Nitrates
ATP sensitive potassium channel openers
If channel blockers
43
Q

What are thrombolytic drugs contraindicated for

A

NSTEMI

Unstable angina

44
Q

What are examples of thrombolytic durgs

A

Most drugs target fibrin:
Streptokinase
Anistreplase

45
Q

What is an infarct

A

Area of ischaemic necrosis within a tissue or organ, produced by occulsion of either its arterial supply or its venous drainage

46
Q

Why is venous infarction less common

A

Arrest of flow due to venous obstruction is unusual as most tissues have numerous venous anastamoses

47
Q

Where are venous infarctions likely to occur

A

Thrombosis of mesenteric veins -> intestinal infarction
Thrombosis in the superior sagittal sinus -> brain
Thrombosis in testis or ovary following torsion

48
Q

What happens when bowels infarct

A

Becomes permeable -> develops into peritonitis resulting in gram negative sepsis

49
Q

How are infarcts divides

A

Colour (red/haemorrhagic vs white/anaemic) and presence (septic infarcts) or absence (bland infarcts) or bacterial contamination

50
Q

What are white infarcts

A

Arterial occlusion and in solid tissues e.g. heart, spleen, kidneys

51
Q

What are transmural heart infarcts

A

Ischaemic necrosis involving full or nearly full thickness of the ventricular wall in the distribution of a single coronary artery. Preservation will be thin band of tissue next to endocardium.

52
Q

What do transmural heart infarcts invovle

A

Coronary atherosclerosis - left anterior descending, left circumflex (supplies left lateral wall, right coronary), subseqeutnyl plaque rupture and superimposed thrombosis -> STEMI

53
Q

What are subendocardial infarcts

A

Constitutes an area of ischaemic necrosis limited to the inner one third of the ventricular wall. There is diffuse stenosing coronary atherosclerosis and global reduction of coronary flow but no plaque rupture and no thrombosis. NSTEMI

54
Q

What morphological complications follow MI

A

Pericarditis
Cardiac rupture
Mural thrombosis
Ventricular aneurism

55
Q

What occurs in pericarditis

A

2nd or 3rd day after MI - fibrinous or fibrnohaemorrhagic

56
Q

What occurs in cardiac rupture

A

Mechanical weakness in necrotic and inflamed myocardium
Ventricular free wall 0> haemopericardium or cardiac tamponade
Rupture of intraventricular septum -> left to right sunt
Rupture of papillary muscles -> severe acute mitral incompetence

57
Q

What is an embolism

A

Transfer of abnormal material by the bloodstream and its impaction in a vessel

58
Q

List the types of emboli

A

Fragments of thrombus, material from ulcerating atheromatous plaques, septic emboli, fragment of tumour (gives rise to metastases) growing into a vein, fat globules, air emboli (300ml), parenchyma cell

59
Q

When is a thrombus pale

A

Fast moving blood

60
Q

When is a thrombus red

A

Slow moving blood

61
Q

Where is fat embolism a problem

A

Lung fields, can be diagnosed with urine test, fat embolism in capillaries of brain is fatal

62
Q

Explain DVT and PE

A

Detachment of a thrombus in a systemic vein, usually in deep vein plexus in the leg. large thrombi may be detached en mass -> right side of the heart. Cause sudden blockage of the pulmonary trunk. Death either immediate or after a short period of resp distress

63
Q

Where are fatal emobli derived from

A

Femoral or iliac veins. Commonest around 10th post operative day

64
Q

What is the definition of IBS

A

Recurrent abdo pain or discomfort 3 days per month in the last 3 months, associated with two or more of the following:
Improvement with defecation
Onset associated with a change in frequency of stool
Associated with change in form of stool

65
Q

What is chronic fatigue

A

Persistent or relapsing, debilitating fatigue for at least 6 months

66
Q

What is fibromyalgia

A

Widespread pain index and symptom severity scores. Present for at least 3 months. Does not have a disorder that would otherwise explain the pain

Supporting Life (14 decks)

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