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Heart > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

1
Q

Arteriosclerosis

Arteriolosclerosis

A

Stiffening of the blood vessels with loss of compliance
◉Arteriosclerosis= large and middle arteries
Hyaline arteriolosclerosis and hyperplastic arteriolosclerosis

◉Arteriolosclerosis= small arteries and arterioles
due to the process of atherosclerosis. growing fatty deposits (atheroma) but also lose compliance due to calcification and an increase in fibrous tissue in the vessel wall.

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2
Q

Atherosclerosis

A

A disease of large and medium-sized arteries characterized by
◉endothelial dysfunction,
◉vascular inflammation
◉accumulation of lipids, cholesterol, calcium and cellular debris
within the intima of the vessel wall.

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3
Q

Endothelial Dysfunction

A

inflammatory activationof vascular cells in diseased vessels
Response-to-injury hypothesis
This model views atherosclerosis as a chronic inflammatory response of the arterial wall to endothelial injury

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4
Q

Causes of endothelial injury

A

◉Physical injury or stress as a result of direct trauma or hypertension
◉Turbulent blood flow
◉Circulation of reactive oxygen species (free radicals), e.g., from smoking or air pollutants
◉Hyperlipidaemia (high blood concentrations of LDL or VLDL)
◉Chronically elevated blood glucose levels
◉Homocysteinaemia, an inherited metabolic defect that leads to very high levels of the homocysteine, a metabolite of methionine; high concentrations are toxic to the endothelium

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5
Q

What happens during inflammation in Endothelial Cells?

A

◉Disrupted permeability barrier
Increased prod of inflammatory cytokines > permeability
◉>prod of leukocyte adhesion molecules > immune cell recruitment
◉

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6
Q

Types of inflammatory cytokines

A

IL-1, IL-6, IL-8,TNF a

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7
Q

Types of leukocyte adhesion molecules

A

V-CAM, I-CAM,E-Selectin, P-Selectin

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8
Q

What happens during inflammation in Smooth Muscle Cells?

A

◉> prod of inflammatory cytokines
◉> extracellular matrix synthesis
◉> inc migration and proliferation into sub-intima

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9
Q

Stages of Plaque Development

A

Fatty Streak
Plaque development
Plaque Disruption/Rupture

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10
Q

Fatty Streak Development

A

LDL enter permeable endothelium - accumulation in tunica intima and bind to proteoglycans in extracellular matrix - Plasma LDL is oxidised and readily taken up by scavenger receptors on macrophages - transform to lipid laden foam cell. Oxidised LDL release cytokines, GF, - Endothelial cells release chemokines and macrophage - > recruitment. Further inducing of endothelial dysfunction

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11
Q

Plaque Development

A

Cytokines and GF stimulate SMC migration from media to intima and proliferation of SMC and ECM prod. - inflammation reinforced and atheroma formed (fibrofatty lesion) - calcification and continuous fibrosis - apoptosis of SMC > acellular fibrous capsule

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12
Q

RIsk factors for atherosclerosis

A 
Cardiovascular disease risks
◉Non modifiable -
Age
Gender
Ethnicity
Genetics
◉Modifiable 
High BP
Smoking
DM
Physical inactivity
Obesity
High blood cholesterol/ Dyslipidaemia/Hyperlipidaemia

Chlamydia pneumoniae infection

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13
Q

Acute Coronary Syndrome

A

Life-threatening conditions that encompass a continuum ranging fromunstable angina (UA)pectoris to the development of a large acutemyocardial infarction (MI),

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14
Q

MI symptoms

A 
Chest pain - metabolic products activate pain receptors 
Tachycardia 
Dyspnoea
Diaphoresis - >symp tone
Nause/Vomiting >parasymp tone
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15
Q

Cardiac markers

A

Cardiac Troponin I and T - 3-4hrs, remains 10-14dyas

CK-MB - Heart and skeletal muscle -3-6hrs(pk14hrs) ,remains 48-72hrs

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16
Q

Commonly affected Coronary arteries

A

◉Left Anterior Descending Artery (40-50%)- supplies the anterior left ventricle, apex and two thirds of the interventricular septum
◉Right Coronary Artery (30-40%)- supplies the posterior wall of the left ventricle, posterior one third of interventricular septum
◉Left Circumflex Artery (~20%)- supplies the lateral wall of the left ventricle

17
Q

Infarction may be

A

Transmural - Abnormal Q waves

Non-transmural/subendocardial - ST and T wave abnormality

18
Q

MI complications

A

Strokes
Cardiogenic shock
CHF
Cardiac Tamponade - risk of myocardial rupture (3-14days)
Arrhythmias
Pericarditis(1-3day) Dressler’s syndrome 2-10wks
Heart Failure

19
Q

Major causes of ischaemic strokes

A

◉Embolic strokes- a travelling mass/clot blocks blood flow causing ischaemia, may come from heart (valves, LV, LA).
◉Thrombotic strokes- Caused by atherosclerosis, blood vessels get completely occluded by thrombus formation when a plaque ruptures. Common in the middle cerebral artery, carotid and basilar and carotid arteries.
◉Watershed strokes- caused by global hypoperfusion due to carotid atherosclerosis

20
Q

resultant symptoms of plaque rupture in carotid atherosclerosis

A

◉ipsilateral amaurosis fugax (same-sided transient visual loss)
◉retinal infarction
◉contralateral body transient ischaemic attack (TIA)
◉stroke (opposite side).

21
Q

Peripheral Vascular Disease

A

The narrowing or occlusion of arteries outside the heart or brain by atherosclerotic plaque.
Also known as peripheral artery disease.
Inadequate blood flow to the limbs causing ischaemia can be classified as:-
Functional, when blood flow is normal at rest but insufficient during exercise (clinically presents as intermittent claudication).
Critical, when there is a perfusion deficit at rest, presence of pain at rest, trophic lesion to the leg and limb is at risk.

22
Q

Symptoms of PVD

A 
Claudication ( dull, cramping pain)
Buttock pain
Numbness of tingling in leg, foot, toes
Change in skin colour
Change in skin temperature
Impotence
Infections or sore that do not heal
Ulcers
Gangrene
23
Q

Renal Artery Disease

A

build up of atherosclerosis in the renal arteries can lead to stenosis of the artery and ischaemia of the kidney and a fall in the glomerular filtration rate.

24
Q

renal artery stenosis

A

It may be suspected to be a problem if you have:
High blood pressure that begins suddenly or worsens without explanation
High blood pressure that begins before age 30 or after age 50
As renal artery stenosis progresses, other signs and symptoms may include:
High blood pressure
A whooshing sound as blood flows through a narrowed vessel (bruit) due to increased turbulence upstream of stenosis
Elevated protein levels in the urine or other signs of abnormal kidney function
Worsening kidney function during treatment for high blood pressure
Fluid overload and swelling in your body’s tissues
Treatment-resistant heart failure

25
Q

ANS regulation of the heart

A

SNS > adrenaline

PNS < acetylcholine via vagal nerve (if cut >25bpm)

26
Q

Chemical regulation of the heart

A

Hormones: Adrenaline & Tyrosine

Ion concentrations

27
Q

Causes of pericardial effusion

A 
Trauma
MI
Heart surgery
Aortic Dissection
Chronic inflammation 
Cancers
Uremic pericarditis
Hypothyroidism
28
Q

Cardiac tamponade

A

Effusion->pressure - lack of stretch and contraction- HR

29
Q

Symptoms of Cardiac tamponade

A 
Becks triad - JVP+Hypotension+Distant heart sounds
Tachycardia
Coughing
Dyspnoea
Weakness
Light-headedness
Pulsus paradoxus >10mmhg
30
Q

Cardiac tamponade investigation

A

ECG =- Tachycardia, low QRS voltage, Electrical alterans
Echo- swinging heart, excess fluid
Cardiac catheterisation - 4 chambers at equal pressure

31
Q

Cardiac tamponade treatment

A

Pericardiocentesis

Address underlying disease

Heart (9 decks)

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