Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Supporting Life > Vascular Diseases > Flashcards

Vascular Diseases Flashcards

(66 cards)

Start Studying
1
Q

What is the normal thickness of the left ventricular wall

A

14mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the normal thickness of the right ventricular wall

A

Less than 4mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does white in heart muscle represent

A

Necrotic tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is arteriosclerosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is Monckeberg’s medial scloeriss

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is arteriolosclerosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are RF for atherosclerosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is T3 of atheromatous plaque

A

Lesions in the aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the P wave

A

Atrial depolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the QRS complex

A

Ventricular depolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is Q

A

Intraventricular septum depolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is R

A

Main mass depolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is S

A

Base depolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is ST

A

Period of zero potential between ventricular depolarisation and repolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the T wave

A

Ventricular repolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
How is MI diagnosed
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
26
What does cardiac I and T indicate
Myocardium damage
27
How do cardiac muscles contract
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
Why is chest pain felt
Ischaemia->metabolites accumulate in the interstitium of heart muscle->adenosine accumulation so ATP isn't recharged->activate nerve endings
29
What causes angina
Plaque can restrict blood flow to cause stable angina. When stenosis reaches 70%, blood flow can no longer reach demand
30
What are the sensations of MI
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
What is the duration of MI sensation
Less than 30 minutes is angina, over 30 minutes is infarction
32
What causes STEMI
Epicardial coronary artery blockage
33
What happens when an atherosclerotic plaque ruptures
Platelets initiate clotting cascade. Fibrinogen is polymerising to form fibrin, trapping RBCS
34
What does statin do
Lower's cholesterol
35
Why does SOB occur with MI
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
What are the advantages of mechanical reperfusion
Faster Less stroke and bleeds Lower mortality High % reperfusion
37
What is the difference between STEMI and NSTEMI
Reperfusion therapy necessary for STEMI as it indicates a completely blocked artery. In NSTEMI, blood flow is limited by stenosis.
38
What is a T1 MI
Spontaneous MI (plaque rupture, ulceration, erosion or dissection)
39
What is a T2 MI
MI secondary to ischaemic imbalance (endothelial dysfunction, spasm, coronary embolism, tach/brady arrhythmia, anemia, hypoxia, hypotension)
40
What is a T3 MI
MI causing death before biomarkers available
41
What is the assessment steps for suspected MI
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
What are anti-anginal drugs
``` Beta-adrenoreceptor blockers L type calcium channel blockers Nitrates ATP sensitive potassium channel openers If channel blockers ```
43
What are thrombolytic drugs contraindicated for
NSTEMI | Unstable angina
44
What are examples of thrombolytic durgs
Most drugs target fibrin: Streptokinase Anistreplase
45
What is an infarct
Area of ischaemic necrosis within a tissue or organ, produced by occulsion of either its arterial supply or its venous drainage
46
Why is venous infarction less common
Arrest of flow due to venous obstruction is unusual as most tissues have numerous venous anastamoses
47
Where are venous infarctions likely to occur
Thrombosis of mesenteric veins -> intestinal infarction Thrombosis in the superior sagittal sinus -> brain Thrombosis in testis or ovary following torsion
48
What happens when bowels infarct
Becomes permeable -> develops into peritonitis resulting in gram negative sepsis
49
How are infarcts divides
Colour (red/haemorrhagic vs white/anaemic) and presence (septic infarcts) or absence (bland infarcts) or bacterial contamination
50
What are white infarcts
Arterial occlusion and in solid tissues e.g. heart, spleen, kidneys
51
What are transmural heart infarcts
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
What do transmural heart infarcts invovle
Coronary atherosclerosis - left anterior descending, left circumflex (supplies left lateral wall, right coronary), subseqeutnyl plaque rupture and superimposed thrombosis -> STEMI
53
What are subendocardial infarcts
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
What morphological complications follow MI
Pericarditis Cardiac rupture Mural thrombosis Ventricular aneurism
55
What occurs in pericarditis
2nd or 3rd day after MI - fibrinous or fibrnohaemorrhagic
56
What occurs in cardiac rupture
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
What is an embolism
Transfer of abnormal material by the bloodstream and its impaction in a vessel
58
List the types of emboli
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
When is a thrombus pale
Fast moving blood
60
When is a thrombus red
Slow moving blood
61
Where is fat embolism a problem
Lung fields, can be diagnosed with urine test, fat embolism in capillaries of brain is fatal
62
Explain DVT and PE
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
Where are fatal emobli derived from
Femoral or iliac veins. Commonest around 10th post operative day
64
What is the definition of IBS
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
What is chronic fatigue
Persistent or relapsing, debilitating fatigue for at least 6 months
66
What is fibromyalgia
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions