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Pathology - Year 2 AC > Week 3 - Heart And Blood Vessels > Flashcards

Week 3 - Heart And Blood Vessels Flashcards

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1
Q

What is atherosclerosis?

A

The progressive narrowing and hardening within an artery potentially resulting in a complete blockage

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2
Q

Why might atherosclerosis be caused?

A
  • initiated by chronic injury to the endothelium –> resulting in chronic inflammation
  • causes of injury - hyperlipidaemia, disturbed flow, smoking, hypertension
  • then progresses as wbc, fat and blood constituents infiltrate injury. Lesion progression sustained by interaction between modified lipoproteins, macrophages, T cells and normal cellular constituents of the blood
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3
Q

What are the 6 stages of atheroma?

A

-initial lesion (isolated macrophage foam
cells)
-fatty streak lesion (mainly intracellular accumulation)
-intermediate lesion (type II changes with small extra cellular lipid pools)
-atheroma lesion (type II changes and core of EC lipid)
-fibroatheroma lesion (lipid core and fibrotic layers, or mainly calcified or mainly fibrotic)
-complicated lesion (surface defect, haematoma -haemorrhage, thrombus

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4
Q

Which arteries do heart attacks and angina (ischaemic heart disease) usually effect?

A

Coronary arteries

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5
Q

Which artery is an aneurysm most likely to effect?

A

The aorta

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6
Q

Which arteries may narrow, causing a stroke?

A

Carotid arteries

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7
Q

Atherosclerotic plaques develop slowly but what may they acutely cause symptoms due to?

A
  • aneurysm and rupture
  • thrombosis
  • haematoma formation
  • embolisation
  • development of critical stenosis
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8
Q

What are collateral vessels?

A

Collateral vessels are extra blood vessels that connect portions of the same artery or link two different arteries. These alternate blood circulation routes develop in most people and are usually closed to the flow of blood. The collateral vessels can be microscopic or they may grow larger.

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9
Q

What is stenosis?

A

the abnormal narrowing of a passage in the body

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10
Q

Which way do atheromas usually grow?

A

Outward (away from lumen)

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11
Q

What causes thrombosis?

A

Rupture of the atheroma plaque’s fibrous cap

-allows blood coagulant factors to contact thrombogenic collagen found in the arterial extracellular matrix and tissue factor produced by macrophage-derived foam cells in the lipid core of lesions

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12
Q

What does atheroma plaque rupture often form?

A

The nidus for thrombi

Nidus - where something originates

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13
Q

What does the normal artery wall possess in order to resist thrombosis and lyse clots that begin to form?

A

-fibrinolytic or antithrombic mechanisms

(thrombomodulin, tissue and urikase-type plasminogen activators, heparan sulphate, proteoglycans, prostacyclin, nitric oxide)

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14
Q

When might the natural fibrinolytic or antithrombic mechanisms in the arteries not work?

A

When the clot overwhelms the endogenous fibrinolytic mechanisms - may propagate and lead to arterial occlusion

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15
Q

What do the consequences of arterial occlusion depend on?

A
  • the degree of existing collateral vessels (pts with chronic multi vessel, occlusive coronary artery disease - these have often formed)
  • in these circumstances, total occlusion may not cause MI
  • pt with less advance disease and without substation stenotic lesions to provide a stimulus for collateral vessel formation - sudden plaque rupture and occlusion produces ST-segment elevation infarction
  • MI/sudden death
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16
Q

What is ischaemic heart disease?

A

Imbalance between supply (perfusion) and demand of the heart for oxygenated blood

-not only low oxygen but also low nutrient substrates and inadequate removal of metabolites

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17
Q

What may cause a lower flow/not flow of oxygenated blood?

A
  • atheroma
  • embolism
  • spasm
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18
Q

What may cause a higher demand for oxygen?

A
  • thyrotoxicosis

- myocardial hypertrophy (e.g. Hypertension)

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19
Q

What are the fixed risk factors for ischaemic heart disease?

A
  • positive family history
  • male sex
  • age
  • genetic factors (like ACE gene deletion)
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20
Q

What are the signs and symptoms of ischaemic heart disease?

A
  • Chest pain (often central, crushing, radiating to left arm or into jaw - elderly or diabetics may not get chest pain)
  • SOB
  • palpitations
  • syncope - temporary loss of consciousness caused by a fall in BP
  • nauseous, sweating, pale
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21
Q

What is the difference between stable and u stable angina?

A

Stable -

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22
Q

What conditions are under ACS - acute coronary syndrome?

A

Unstable angina
STEMI
NSTEMI

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23
Q

What’s the difference between STEMI AND NSTEMI?

A

-both MI

ST segment elevation myocardial infarction (STEMI) - most serious type of heart attack, where theres a long interruption to the blood supply, usually caused by a total blockage of the coronary artery, which can cause extensive damage to a large area of the heart.

non-ST segment elevation myocardial infarction (NSTEMI) - can be less serious because supply of blood to the heart is only partially blocked resulting in a smaller section of the heart being damaged (still regarded as a serious medical emergency)

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24
Q

What are the investigations conducted to text for angina and ACS?

A 
Observations -BP, pulse, RR, sats
Bloods - inc. cardiac enzymes 
Chest X-ray 
ECG
Exercise tolerance test
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25
What are the complication s that can occur because of an MI?
- cardiac arrest - arrhythmias - pericarditis - valvular defects - ventricular wall rupture - DVT - pulmonary embolus)
26
What is the immediate and common treatment for all ACS events and angina?
- oxygen - pain relief - aspirin
27
What is the most common treatments of angina?
Change of lifestyle, nitrates (dilates vasculature), B-blockers
28
What is the most common treatments for ACS?
Thrombolytic therapy, PTCA (percutaneous transluminal coronary angioplasty), CABG (coronary artery bypass graft), drugs
29
What is hyperlipidaemia?
High level of fat in the blood - LDL cholestorol (bad) - delivered to peripheral tissues - HDL cholesterol (good) -mobilises cholesterol from the tissues and transports it to the liver to be excreted in bile
30
How is hyperlipidaemia treated?
- reduce cholesterol and saturated fat in diet | - role of statins
31
Name some vascular diseases
Atherosclerosis, aneurysms, hypertension, diabetic vascular disease, vein diseases
32
What is cardiac failure?
Heart unable to pump blood at rate required for normal functioning Resulting in: - oedema (pulmonary and peripheral) - tiredness Initially the heart compensates -leading to cardiac hypertrophy and/or dilation and eventual inability to maintain normal function
33
State the causes of cardiac failure
Ischaemic heart disease, hypertension, valvular heart disease, arrhythmias, congenital heart disease
34
What are the symptoms of cardiac failure?
- SOB - fatigue - fluid in lungs (pulmonary oedema) - all over, excessive, fluid filled veins (systemic venous congestion and oedema)
35
What are the classifications of cardiac failure?
- acute vs. chronic | - left vs. right vs. both sided (congestive)
36
How is cardiac failure treated?
- treat underlying cause | - range of medicines used to control heart failure
37
What does a valve in the heart do?
regulates flow in one direction
38
How many valves are there in the heart?
4 valves/sites
39
State the conditions included in valvular heart disease and which is the most common
Stenosis, incompetence/regurgitation, vegetations -stenoses of the aortic and mitral valves
40
What is stenosis in valvular heart disease?
Failure to open completely, impeding forward flow -mainly due to primary valve cusp abnormality, a chronic process
41
What is incompetence/regurgitation in valvular heart disease?
- failure to close, allowing reverse flow | - may result from disease of cusps but also damage to supporting structures (tendinous cords, papillary muscles)
42
What are vegetations in valvular heart disease?
Abnormal tissue growth on valve (fibrin, platelets and bacteria) -can result from infective endocarditis and rheumatic fever
43
What are the underlying causes of valvular heart disease?
Infection (endocarditis, rheumatic disease), calcification aortic valve disease, age-related degeneration, carcinoid syndrome, fibrosis and muscle rupture after MI, heart failure, hypertension, congenital, prosthetic heart valves, connective tissue disorders, IV drug use
44
What are the symptoms/consequences of vascular disease?
Differ with site/type lesion - stroke - arrhythmias - ventricular hypertrophy - angina - syncope (fainting) - heart failure - infants to kidneys and spleen - poor prognosis once symptoms show
45
What is the endocardium?
Inner lining of the heart and its valves
46
What is endocarditis?
When the lining of the heart/valves becomes inflamed -infection occurs on the edge of heart valves (Vegetation is a mass of bacteria, fibrin and platelets) -usually left sided but right sided in IV drug use
47
What pathogen usually effects abnormal valves usually after dental extraction/cleaning/bronchoscopy/tonsillectomy?
Streptococci (a-haemolytic) Staph aureus affects previously normal valves - usually IV drug abusers
48
What is it important to do for those at risk of developing endocarditis?
Prophylaxis -imperative to give abx to those at risk of developing endocarditis prior to any procedure that may produce a bacteraemia
49
What are the symptoms of endocarditis?
Sepsis Heart failure New murmur
50
What is pericarditis and myocarditis?
Inflammatory reaction involving the heart sac or heart muscle
51
What can cause pericarditis?
Virus, bacteria, parasitic, TB, uraemia (urine products in blood)
52
What can cause myocarditis?
Carcinoma, MI, post-surgery, drugs, connective tissue disease, Unknown, radiation
53
What types of pericarditis and myocarditis can you get?
Acute and chronic
54
What are the symptoms and signs of pericarditis and myocarditis?
Chest pain | Cardiac failure
55
How is pericarditis and endocarditis treated?
Anti-inflammatory drugs | Surgical excision of the pericardium
56
Name some unusual cardiac diseases
Cardiomyopathy, multisystem diseases (e.g. Sarcoidosis and amyloidosis), thyrotoxicosis, myxoedema, alcoholism, pregnancy, iatrogenic (drug induced disease)
57
What is cardiomyopathy?
Disease of the heart muscle Cardiac dilation Hypertrophic cardiomyopathy Restrictive cardiomyopathy
58
What is cardiac dilation?
Cardiacmyopathy Process of expansion/stretching: - dilation of chambers - heart large and flabby
59
What is hypertrophic cardiomyopathy?
-heavy, muscular, hypercontracting - abnormal diastolic filling - 1/3 have intermittent left ventricular outflow obstruction - end stage dilation can occur
60
What are the clinical features of hypertrophic cardiacmyopathy?
- SOB - chest pain - palpitations - blackout - sudden death - AF - thickened myocardium due to increase in the size of myocardial cells, septal hypertrophy characteristic of HCM
61
What is an aneurysm?
Localised, permanent, abnormal dilation of a blood vessel
62
What can cause an aneurysm?
Age, atherosclerosis, ischaemia, hypertension, inflammation, diabetes, autoimmune diseases, bacteria, bacterial endocarditis, fungus, Marfan's syndrome, syphilis
63
How can an aneurysm be treated?
Stents, surgery, reducing arterial pressure
64
What is hypertension?
High BP
65
What is hypertension classified into?
Causes: - primary (essential) hypertension (95%) - secondary hypertension (5-10%) Further classified clinically: - benign hypertension - malignant hypertension
66
What are the risk factors for hypertension?
Non modifiable - genetics Modifiable - diet (high Na+ intake), lifestyle (stress + lack of exercise), weight, alcohol, smoking
67
What are some causes of secondary hypertension?
- renal e.g. polycystic kidney disease - endocrine e.g. thyrotoxicosis - vascular e.g. raised intravascular volume - neurogenic e.g. acute stress - surgery
68
What is benign hypertension?
- most remain stable over many years - live a relatively normal life - until/unless complications arrive
69
What is malignant hypertension?
- accelerated hypertensive disease - 5% of cases - rapidly rising BP - 90% die in first year
70
What complications of hypertension arise in the blood vessels?
Large blood vessel disease (macroangiopathy) - atherosclerosis Small blood vessel disease (microangiopathy) -arteriolosclerosis Increased risk of rupture and dissection and MI
71
What complications of hypertension arise in the heart?
Heart disease - left ventricular hypertrophy - cardiac failure - MI
72
What complications of hypertension arise in the kidneys?
Benign nephrosclerosis | Renal failure
73
What complications of hypertension arise in the eyes (retina)?
Hypertensive retinopathy ``` Retinopathy grades: 1 - thickening of arterioles 2 - arteriolar spasms 3 - haemorrhages 4 - papilloedema (seen in malignant hypertension) ```
74
What complications of hypertension arise in the brain?
``` Cerebral haemorrhage Cerebral infarction (stroke) ```
75
What is diabetic vascular disease and what damage can occur?
- damage to vessels generally - atherosclerosis | - damage to kidneys, nerves, retinas (retinopathy)
76
What complications can arise with diabetic vascular disease?
Gangrene Renal failure Blindness
77
What reduces diabetic vascular disease?
Effective control of diabetes
78
What is venous thrombosis (e.g. DVT)?
When normal venous return is impeded -predisposes to thrombosis
79
What can cause venous thrombosis (e.g. DVT)?
Immobility, malignancy, pregnancy/child birth, oestrogens, haematological disorders, IV cannulas
80
What is there a danger of when you have a venous thrombosis?
Pulmonary embolism
81
What are varicosities?
Tortuous and distended veins -common problem
82
What can be the cause of varicosities?
- incompetent valves in legs - impaired venous return - stasis - oedema - fibrin deposits around veins -often associated ulceration -ankles and legs
83
Name the most common types of congenital cardiovascular disease
- septal defects - failure of blood vessel closure at birth (patent ductus arteriosus) - narrowed aorta -coarctation of the aorta - valvular abnormalities - vessels the wrong way round - coronary artery defects - multiple defects - fallot's tetralogy
84
What is atheroma and where does it occur?
Build up of fatty material on the inside wall of an artery - slowly progressive - lower abdominal aorta, coronary arteries, popliteal arteries, internal carotid arteries and vessels of circle of Willis

Pathology - Year 2 AC (19 decks)

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