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Cardiovascular (Annie) > Clinical aspects of CV risk > Flashcards

Clinical aspects of CV risk Flashcards

1
Q

what is atherosclerosis?

A

a progressive disease that is characterised by a build-up of plaque within the arteries

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2
Q

how can plaque be formed?

A
  • fatty substances
  • cholesterol
  • cellular waste
  • calcium
  • fibrin
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3
Q

what are the 2 ways that plaques can block blood flow through artery?

A

1) PARTIALLY BLOCK blood flow through an artery

1) TOTALLY BLOCK blood flow through an artery

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4
Q

what 2 things can happen to the plaque?

A

1) bleeding into the plaque
2) formation of a clot on the surface of the plaque
= blocking the artery

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5
Q

what 2 things can happen as a result from atherosclerosis?

A

1) heart attack

2) stroke

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6
Q

in the pathogenesis of atherosclerotic plaques, what happens after endothelial damage?
- give examples.

A

= protective response results in production of cellular adhesion molecules such as cytokines (e.g. interleukin 1, TNF-alpha), chemokines (IL8) and growth factors.

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7
Q

in pathogenesis of atherosclerotic plaques, what happens after the protective response resulting in production of cellular adhesion molecules?

A

= monocytes and T lymphocytes (inflammatory cells) attach to ‘sticky’ surfaces of endothelial cells

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8
Q

in pathogenesis of atherosclerotic plaques, what happens after monocytes and T lymphocytes attach to sticky surfaces of endothelial cells?

A

= inflammatory cells migrate through arterial wall to sub-endothelial space

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9
Q

in pathogenesis of atherosclerotic plaques, what happens after migrate through arterial wall to sub-endothelial space?

A

= monocytes differentiate into macrophages where they take up oxidised LDL-C

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10
Q

in pathogenesis of atherosclerotic plaques, what happens after macrophages are up oxidised LDL-C?

A

= oxidised LDL promotes death of endothelial cells & inflammatory response causing
= LIPID RICH FOAM CELLS

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11
Q

n pathogenesis of atherosclerotic plaques, what happens after lipid rich foam cells?

A

= fatty streak & plaques

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12
Q

what is the primary event in atherosclerosis thought to be and what causes this primary event?

A

thought to be damage to the endothelium of arterial walls, causing endothelial dysfunction

Caused by;

  • haemo-dynamic factors (shear stress causing by hypertension)
  • vasoactive substances
  • mediators (cytokines) from blood cells
  • smoke
  • bad diet
  • elevated glucose levels
  • oxidised LDL-C
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13
Q

what is athero-thrombosis?

A

= formation of acute thrombus (blood clot) in a vessel affected by atherosclerosis

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14
Q

how is athero-thrombosis initially initiated?

then what happens?

A

Initiated by;
= changes in vessel wall resulting from plaque disruption
= atheroscloritc plaques becomes unstable & rupture, exposing components like collagen…allowing platelets to adhere to the damaged area & initiate thrombus formation

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15
Q

what can a thrombus do?

A

= extend or occlude the vessel, causing acute ischema & tissue injury.
- fatal or non-fatal CV events e.g. stroke, MI, peripheral artery occlusion which could lead to ischemia

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16
Q

what are some MODIFIABLE risk factors of developing atherosclerotic plaques?

A

1) smoking
2) dyslipidaemia
- raised LDL cholesterol
- raised triglycerides
- low HDL cholesterol

3) raised blood pressure
4) diabetes mellitus
5) obesity
6) dietary factors
7) thrombogenic factors
8) lack of exercise
9) excessive alcohol consumption
10) deprivation
11) inactivity

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17
Q

what are NON-MODIFIABLE risk factors of developing atherosclerotic plaques?

A

1) age
2) gender
3) family history of coronary heart disease
4) person history of coronary heart disease

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18
Q

what are the 5 classifications of lipoproteins in order from lowest density to highest?

A

1) chylomicrons
2) VLDL (very low density lipoproteins)
3) IDL (intermediate density lipoproteins)
4) LDL (low density lipoproteins)
5) HDL (high density lipoproteins)

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19
Q

Yes or No.
Are chylomicrons associated with atherosclerosis?

  • where are chylomicrons synthesised?
  • what do they transport?
A

No.

Synthesised;
= in gut after a fatty meal

Transport;
= they transport dietary triglyceride from gut to sites of use & storage, & are cleared rapidly from bloodstream

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20
Q

Where are VLDL lipoproteins produced and what do they do?

Why are VLDL implicated in atherosclerosis?

A

Synthesised
= in the liver

Function;
= main carriers of endogenous triglycerides & cholesterol to sites for use or storage

Atherosclerosis;
= as VLDL are involved in the synthesis of LDL & HDL

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21
Q

when are IDL lipoproteins formed?

A

formed;

= formed during the breakdown of VLDL & chylomicrons

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22
Q

In comparison to VLDL, do IDL contain more or less triglyceride & cholesterol?

A

IDL = contain less triglyceride & more cholesterol than VLDL

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23
Q

Yes or No.

Are ILD lipoproteins involved in atherosclerosis?

A

Yes - they are involved.

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24
Q

what are LDL generated from?

A

Generated;

= from IDL in circulation

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25
Q

what lipoprotein is the principle lipoprotein involved in arteriosclerosis and why?

A

LDL

= because they are the main carriers of cholesterol

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26
Q

what is the most atherogenic form LDL?

A

oxidised LDL

27
Q

does HDL cause atherosclerosis?

A

no

- they protect against is development

28
Q

What 2 diseases is LDL cholesterol strongly associated to?

A

1) atherosclerosis

2) coronary heart events

29
Q

what 4 factors modify LDL cholesterol?

A

1) low HDL cholesterol
2) smoking
3) hypertension
4) diabetes

30
Q

what diseases are associated with triglycerides?

- whats its relationship to HDL and LDL levels?

A

increased risk of CHD events

- related to LOW HDL levels & HIGHLY ATHEROGENIC forms of LDL cholesterol

31
Q

what is normal triglyceride levels and what are high triglyceride levels?

A

normal = 2.3mmol/l

high = 11.3mmol/l
= increased pancreatitis risk

32
Q

what role does HDL cholesterol do?

A

= protective effect for risk of atherosclerosis and CHD

33
Q

what is the relationship between HDL levels and risk for atherosclerosis and CHD?

A
  • lower the HDL cholesterol level, the higher the risk for atherosclerosis and CHD
    = low level, increases risk
34
Q

when does HDL cholesterol trend to be low?

A

when triglycerides are high

35
Q

when is the level of HDL lowered?

A
  • smoking
  • obesity
  • physical inactivity
36
Q

in the endogenous pathway of lipid metabolism, what particles transports tri-glycerides and cholesterol from liver to rest of the body?

A

VLDL

37
Q

what happens to VLDL?

A
  • it undergoes dilapidation with the enzyme lipoprotein lipase
38
Q

in the endogenous pathway, what happens to the triglycerides?

A
  • they are removed from the core & exchanged for cholesterol esters, principally HDL.
39
Q

in the endogenous pathway, what is most of VLDL transformed into?
- what enzyme facilities this transfer in large VLDL particles and small VLDL particles?

A

= LDL

Large VLDL particles = lipoprotein lipase

Small VLDL = hepatic lipase

40
Q

In the exogenous pathway, what happens to the dietary fats?

A
  • they are broken down in GI tract into cholesterol & fatty acids and tri-glyerides
41
Q

in the exogenous pathway, what happens to most of the triglycerides?
what happens after this absorption?

A
  • virtually all triglycerides are absorbed to form CHYLOMICRONS which enter bloodstream to be transported to liver.
42
Q

in the exogenous pathway, what happens to he chylomicrons formed?

A
  • chylomicrons are hydrolysed by enzyme lipoprotein lipase releasing energy production or storage
  • chylomicrons undergo further dilapidation, resulting in formation of chylomicrons remnants.
43
Q

what is the primary target to prevent CHD?

A

LDL-C

44
Q

what do statins do?

A

= always reduce coronary heart disease end points

= reduces total cholesterol & LDL cholesterol

45
Q

what other effects does statin cause?

A
  • improvement of endothelial dysfunction
  • increased nitric oxide bioavailability
  • antioxidant properties
  • inhibition of inflammatory response
  • stabilisation of atherosclerotic plaques
46
Q

what are xanthelasma’s?

A

= xanthomas of eyelids that may or may not be associated with hyper-lipidemia

47
Q

where are tendon xanthomas found?

A

= extensor tendons of;

  • fingers
  • patella
  • elbows
  • achilles tendon (common)
48
Q

what infiltrates the tendon in tendon xanthomas?

A

= lipids;

  • hypercholestterolemia; types I & II
  • normal lipids; cerebrotendinous xanthomatosis; plant sterols
49
Q

what is tuberous xanthomas?

A 
= lipid deposits in; 
- dermis & sub-cutis
- papular
- nodular or plaques
- extensor surfaces of large joints
- hands
- buttock
-  heels
- flexures 
= familial or acquired hyper-tri-glycereidemias; biliary cirrhosis
50
Q

what is eruptive xanthomas?

A

= small reddish yellow papules; buttocks, posterior things or body folds

51
Q

what causes eruptive xanthomas?

A

usually abrupt increase in serum triglyceride levels

52
Q

what are possible diseases attributed to hypertension?

A
  • heart failure
  • left ventricular hypertrophy
  • MI
  • coronary heart disease
  • stroke
  • hypersensitive encephalopathy
  • cerebral haemorrhage
53
Q

what are the 2 types of hypertension and wha causes them?

A

1) essential hypertension
= no underlying cause

2) secondary hypertension
= underlying cause

54
Q

what 3 things does hypertension treatment?

A

1) reduces ischaemic heart disease
2) reduces stroke
3) redues mortality

55
Q

what lifestyles medication can be made to lower hypertension?

A
  • lose weight
  • limit alcohol intake
  • increase physical activity
  • reduce salts intake
  • stop smoking
  • limit intake of foods rich in fats & cholesterol
56
Q

for microvascular complications, when does the clock start ticking?

A

= at onset of hyperglycaemia

57
Q

for macro-vascular complications, when does the clock start ticking?

A

= before diagnosis of hyperglycaemia

58
Q

what 5 things should a healthy diet contain?

A
  • micronutrients
  • antioxidants
  • omega 3 & 6
  • polyunsaturates
  • mono-saturates
59
Q

what is metabolic syndrome?

A

= cluster of biochemical and physiological abnormalities associated with the development of CV disease and type 2 diabetes.

60
Q

what are the 5 risk factors for metabolic syndrome?

- and what are the defining levels for each.

A

1) abdominal obesity
- waste circumference

2) triglycerides
- > 1.7mmol/l

3) HDL-C
- < 1mmol/l in men
- < 1.3mmol/l in women

4) Blood pressure
- > 130/>85mmHg

5) fasting glucose
- > 5.6mmol/l

61
Q

what ethnic group has a higher & lower death rate for CHD?

A

South asians = higher death rate

Black Caribbean & black africans = lower death rate

62
Q

how do you treat ischaemia?

A

1) anti-anginal medications
- calcium blokers
- beta blockers
- nitrates

2) re-vascularization
- angioplasty
- CAGB

63
Q

how do you treat atherothtrombosis?

A
  • statins
  • aspirin
  • beta blockers
  • ACE inhibitors
  • exercise
  • smoking cessation

Cardiovascular (Annie) (36 decks)

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