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C. Year 3 MLA Cardiovascular Conditions/Diseases > Dyslipidaemia > Flashcards

Dyslipidaemia Flashcards

1
Q

What is a lipoprotein?

1 - molecule composed of lipids
2 - molecule composed of proteins
3 - molecule containing lipids and proteins

A

3 - molecule containing lipids and protein

  • proteins allows lipids to be transported in blood
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2
Q

Which of the following are the main components of lipoproteins?

1 - cholesterol esters
2 - triglycerides
3 - apoproteins
4 - phospholipids
5 - all of the above

A

5 - all of the above

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3
Q

Where is the majority of the cholesterol in the body produced, the liver or adipose cells?

A
  • liver
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4
Q

What is 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA)?

A
  • intermediate precursor of cholesterol
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5
Q

What is the rate limiting step and the target of statins in an attempt to reduce cholesterol synthesis?

1 - fatty acid synthase
2 - 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase
3 - HMG-CoA synthase
4 - acetyl-coA carboxylase

A

2 - 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase

  • HMG-CoA converted to Mevalonate which can then enter the melanovate cycle to make cholesterol
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6
Q

What is the basic principle of exogenous lipid transport?

1 - transport TAGs throughout the body
2 - transport cholesterol to the body
3 - transport cholesterol from body to liver
4 - transport TAGs and cholesterol from the GIT to the liver

A

4 - transport TAGs and cholesterol from the GIT to the liver

  • processed into chylomicrons
  • GIT to lymphatics to liver
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7
Q

Once cholesterol has been synthesised in the liver, it is once again packed up into lipoproteins and sent off into the circulation to carry TAGs to the rest of the body as part of the endogenous. Which type of lipoprotein is used 1st?

1 - chylomicrons
2 - LDL
3 - HDL
4 - VLDL

A

4 - VLDL

  • low density refers to the concentration of cholesterol
  • VLDL = high TAGs and low cholesterol
  • LDL = low TAGs and high cholesterol
  • lipoprotein lipase released from capillaries - triglycerides released from chylomicrons
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8
Q

Once VLDL have been distributed around the body and distributed TAGs they become LDLs (distribute cholesterol around the body as part of the endogenous), and ultimately HDLs. What is the benefit of HDLs?

1 - remove excess TAGs from blood
2 - collect excess cholesterol and return it to the liver
3 - remove cholesterol from plaques
4 - distribute cholesterol around the body

A

2 - collect excess cholesterol and return it to the liver

  • part of the reverse pathway
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9
Q

In endogenous lipid transport very low density lipoproteins (VLDL) are created and released from the liver into the circulation. What is the first thing that happens to them in the capillaries?

1 - processed into LDL
2 - more throughout blood for lipoprotein lipase to digested TAGs and release fatty acids
3 - processed in HDL
4 - move directly to adipose cells to deposit TAG and cholesterol

A

2 - more throughout blood for lipoprotein lipase to digested TAGs and release fatty acids

  • lipoprotein lipase is released from capillaries
  • TAG and fatty acids are released from VLDL and absorbed by capillaries
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10
Q

In endogenous lipid transport once very low density lipoproteins (VLDL) have had most of their TAGs absorbed by capillaries, what do VLDL become?

1 - chylomicrons
2 - intermediate lipoproteins (IDL)
3 - LDL
4 - HDL

A

2 - intermediate lipoproteins (IDL)

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11
Q

In endogenous lipid transport what happens to the intermediate lipoproteins that are formed from VLDL?

1 - repackaged in liver to HDL
2 - repackaged in liver to VLDL
3 - repackaged in liver to LDL
4 - repackaged in liver to bile acids

A

3 - repackaged in liver to LDL

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12
Q

In endogenous lipid transport what happens to low density lipoproteins (LDL)?

1 - transport TAGs throughout the body
2 - transport cholesterol to the body
3 - transport cholesterol from body to liver
4 - transport TAGs and cholesterol from the GIT to the liver

A

2 - transport cholesterol to the body

  • LDLs are transported to peripheries
  • LDL receptors bind to LDL
  • cholesterol is stored in tissues
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13
Q

What is the reverse pathway involved in lipid transport?

1 - remove excess TAGs from blood
2 - collect excess cholesterol and return it to the liver
3 - remove cholesterol from plaques
4 - distribute cholesterol around the body

A

2 - collect excess cholesterol and return it to the liver

  • free cholesterol in tissues is absorbed by HDL
  • HDL transport cholesterol to liver for processing
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14
Q

Out of the 5 main lipoproteins:

  • chlylomicrons
  • VLDL
  • IDL
  • LDL
  • HDL

Which has the highest cholesterol and TAG content?

A
  • VLDL = highest TAG content
  • LDL = highest cholesterol content
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15
Q

Primary dyslipidaemia is a dysfunction in lipid metabolism that causes elevated lipid profile. What is the cause of primary dyslipidaemia?

1 - abnormality of lipoprotein metabolism
2 - excess cholesterol intake
3 - excess synthesis of cholesterol by the liver
4 - all of the above

A

1 - abnormality of lipoprotein metabolism

  • generally due to genetics
  • abnormal enzymes, abnormal lipoprotein structure or lack of or dysfunctional lipoprotein receptors
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16
Q

Which of the following are causes of primary dyslipidaemia?

1 - abnormal enzymes
2 - abnormal lipoprotein structure
3 - lack of or dysfunctional lipoprotein receptors
4 - all of the above

A

4 - all of the above

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17
Q

What is the Frederick classification?

1 - classification of arrhythmias
2 - classification of hypertension
3 - classification of heart failure
4 - classification of dyslipidaemia

A

4 - classification of dyslipidaemia

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18
Q

Which of the following is NOT a key characteristic of type I familial hyperchylomicroanaemia, according to the Frederick classification?

1 - low chylomicrons
2 - primary cause lipoprotein lipase
3 - normal cholesterol
4 - high TAGs

A

1 - low chylomicrons

  • associated with high chylomicrons as per the name
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19
Q

Which of the following is NOT a key characteristic of type IIa familial hypercholesterolaemia, according to the Frederick classification?

1 - high LDL
2 - primary cause lipoprotein lipase
3 - normal, or slightly raised TAGs
4 - high cholesterol (>5mmol/L even at birth)

A

2 - primary cause lipoprotein lipase

  • primary cause is LDL receptors on tissues
  • there is either none or very few
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20
Q

Are young patients with type IIa familial hypercholesterolaemia at risk of atherosclerosis?

A
  • yes
  • HIGH RISK of atherosclerosis
  • need aggressive treatment
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21
Q

What type of inheritance is hypercholesterolaemia type IIa?

1 - autosomal (non sex chromosome specific) dominant
2 - autosomal recessive
3 - X linked dominant
4 - X linked recessive

A

1 - autosomal (non sex chromosome specific) dominant

  • 1 inherited gene = bad
  • 2 inherited genes = really bad
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22
Q

How common is familial hypercholesterolaemia type IIa?

1 - 0.5% of population
2 - 10% of population
3 - 20% of population
4 - >35% of population

A

1 - 0.5% of population

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23
Q

Which of the following is NOT a key characteristic of type IIb familial combined hyperlipidaemia, according to the Frederick classification?

1 - high LDL and VLDL
2 - primary cause is high Apo B 100
3 - low TAGs
4 - high cholesterol

A

3 - low TAGs

  • TAGs will be modernly raised
  • metabolic syndrome is common in these patients as all bad lipids are high (VLDL, LDL and TAG)
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24
Q

What type of inheritance is combined hyperlipidaemia type IIb?

1 - autosomal (non sex chromosome specific) dominant
2 - autosomal recessive
3 - X linked dominant
4 - X linked recessive

A

1 - autosomal (non sex chromosome specific) dominant

  • 1 inherited = bad
  • 2 inherited = really bad
  • can be a number of genetic causes
25
Q

How common is familial combined hyperlipidaemia type IIb?

1 - 0.5% of population
2 - 10% of population
3 - 20% of population
4 - >35% of population

A

2 - 10% of population

  • most common form
26
Q

What are 2 very common clinical presentations, what may be useful in identifying a patient with familial combined hyperlipidaemia type IIb?

1 - insulin resistance
2 - obesity
3 - CKD
4 - liver fibrosis

A

1 - insulin resistance
2 - obesity

27
Q

In familial combined hyperlipidaemia type IIb what is the most common apolipoprotein affected?

1 - A-100 (ApoA-100)
2 - B-100 (ApoB-100)
3 - C2-100 (ApoC2-100)
4 - all of the above

A
  • mutated apolipoprotein B-100 (ApoB-100)
  • overproduction of ApoB-100
  • common in LDL and VLDL
28
Q

What % of premature IHD does familial combined hyperlipidaemia type IIb accounts for?

1 - 0.2%
2 - 2%
3 - 20%
4 - 40%

A

3 - 20%

  • premature is anyone <70 y/o
29
Q

Which of the following is NOT a key characteristic of type III familial dysbetalipoproteinaemia, according to the Frederick classification?

1 - high IDL and chylomicrons
2 - primary cause is high Apo B 100
3 - moderately high TAGs
4 - high cholesterol

A

2 - primary cause is high Apo B 100

  • primary cause is Apo E mutation
  • very rare
30
Q

Which of the following is NOT a key characteristic of type IV familial hypertriglyceridaemia, according to the Frederick classification?

1 - high LDL and HDL
2 - primary cause is unknown
3 - high TAGs (>5mmol/L)
4 - normal cholesterol (may be high)

A

1 - high LDL and HDL

  • elevated lipoproteins are VLDL
31
Q

How common is type IV familial hypertriglyceridaemia?

1 - 1%
2 - 10%
3 - 20%
4 - 40%

A

1 - 1%

32
Q

Which of the following conditions is associated with type IV familial hypertriglyceridaemia?

1 - gall stones
2 - liver fibrosis
3 - acute pancreatitis
4 - ileus

A

3 - acute pancreatitis

  • due to pancreatic capillary obstruction
  • occurs when TAGs >10mmol/L
33
Q

What of the following are common clinical presentations of patients with familial hypertriglyceridaemia type IV?

1 - insulin resistance
2 - obesity
3 - eruptive xanthomas
4 - all of the above

A

4 - all of the above

34
Q

Of the 5 types of dyslipidaemia below, which 3 account for 95% of all primary dyslipidaemias?

1 - Type I Familial hyperchylomicronaemia
2 - Type IIa Familial hypercholesterolaemia
3 - Type IIb Familial combined hyperlipidaemia
4 - Type III Familial dysbetalipoproteinaemia
5 - Type IV Familial hypertriglyceridaemia

A

2 - Type IIa Familial hypercholesterolaemia
3 - Type IIb Familial combined hyperlipidaemia
5 - Type IV Familial hypertriglyceridaemia

35
Q

What is xanthelasmata?

1 - fatty build up in tendons
2 - fatty build up around eyes
3 - fatty build on palms of hands
4 - fatty build up causing itchy red spots on skin

A

2 - fatty build up around eyes

  • normally macrophages that contain lipids
36
Q

What is tendon xanthoma?

1 - fatty build up in tendons
2 - fatty build up around eyes
3 - fatty build on palms of hands
4 - fatty build up causing itchy red spots on skin

A

1 - fatty build up in tendons

37
Q

What is palmar xanthoma?

1 - fatty build up in tendons
2 - fatty build up around eyes
3 - fatty build on palms of hands
4 - fatty build up causing itchy red spots on skin

A

3 - fatty build on palms of hands

38
Q

What is eruptive xanthoma?

1 - fatty build up in tendons
2 - fatty build up around eyes
3 - fatty build on palms of hands
4 - fatty build up causing itchy red spots on skin

A

4 - fatty build up causing itchy red spots on skin

  • red/pink lumps - itchy and raised
  • common in hypertriglyceridaemia
39
Q

What are the 2 most common risk scores used in the UK?

1 - Q-Risk
2 - JBS3
3 - Framlington risk score
4 - AHA risk score

A

1 - Q-Risk
2 - JBS3

40
Q

Which cardiovascular risk score do NICE recommend using?

1 - Q-Risk
2 - JBS3
3 - Framlington risk score
4 - ASCVD risk score

A

1 - Q-risk

41
Q

What is the purpose of the Q-risk score?

1 - risk assessment of CV event in <10 y
2 - lifetime risk assessment of CV event
3 - risk assessment of CV event in <50 y
4 - risk assessment of CV event in >65 y/o

A

1 - risk assessment of CV event in <10 y

  • > 10% risk should be started on statins
42
Q

What is the only drug indicated for primary prevention of a cardiovascular event based on risk score?

1 - B-blockers
2 - statins
3 - ACE-I
4 - loop diuretics

A

2 - statins

43
Q

Patients prescribed statins should be assessed at 3 months for response. What is the aim in reduction in LDL?

1 - reduced by 10%
2 - reduced by 20%
3 - reduced by 40%
4 - reduced by >65%

A

3 - reduced by 40%

44
Q

Typically when do we normally treat hypertension?

1 - >140/90
2 - >160/100
3 - >180/110
4 - >200

A

2 - >160/100

  • or >150/95 mmHg when using 24 hour ambulatory BP, or home BP monitoring
45
Q

Typically we treat stage 2 hypertension, >160/100 or >150/95 mmHg when using 24 hour ambulatory BP, or home BP monitoring. However, if we account for the Q-risk >10%, what blood pressure would we begin treating?

1 - >140/90
2 - >160/100
3 - >180/110
4 - >200

A

1 - >140/90

  • or >135/90 mmHg when using 24 hour ambulatory BP, or home BP monitoring
46
Q

In ageing do we generally see a dramatic change in resting cardiovascular function?

A
  • no
47
Q

In ageing we do not generally see a dramatic change in resting cardiovascular (CV) function. Do we see a change in reserve function in CV in ageing?

A
  • yes
  • less able to respond to stressors, such as MI, exercise etc..
48
Q

What is the most striking abnormality in the left ventricle of older patients?

1 - mild hypertrophy
2 - mild and dilation
3 - increased stiffness (‘diastolic dysfunction’)
4 - ejection fraction is blunted in response to exertion

A

3 - increased stiffness (‘diastolic dysfunction’)

  • stiffness is due to fibrosis and altered Ca2+ metabolism
49
Q

As we age the right and left atrium become dilated and stretch more. What does this increase the risk of in the elderly?

1 - stroke
2 - AF
3 - DVT
4 - right sided heart failure

A

2 - AF

50
Q

What happens to the left atrium (LA) in ageing during exertion?

1 - LA pressure increases
2 - LA pressure decreases
3 - LA stops contracting

A

1 - LA pressure increases

  • increases the risk of pulmonary oedema during a stressor of the CV system
51
Q

In ageing typically which 2 valves will have some degree of calcification?

1 - aortic
2 - pulmonary
3 - tricuspid
4 - mitral

A

1 - aortic
- can lead to stenosis

4 - mitral
- can lead to regurgitation

52
Q

In ageing what happens to the pacemaker cells in the SA and AV nodes?

A
  • decreases
  • increases the risk of AF and heart block
53
Q

Ageing patients typically have a similar HR to younger patients, Why is this?

1 - myocytes proliferation
2 - increased sensitivity in pacemaker cells
3 - autonomic control
4 - vagal nerve inhibits HR

A

3 - autonomic control

  • suppresses HR
  • BUT maximum HR is lower as autonomic control inhibits ability to increase HR excessively
  • estimate max HR using 220 - age
54
Q

In the heart of ageing patients there is an altered energy state, with a lower phosphocreatine:ATP ratio. Why is this important?

1 - less ATP available
2 - transport of ATP out of mitochondria is lower
3 - less creatinine available
4 - all of the above

A

2 - transport of ATP out of mitochondria is lower

55
Q

Does the aorta typically get longer and increase in diameter as we age?

A
  • yes
  • BUT stiffness of walls increases
  • increases stress on LV and impairs blood flow to coronary arteries
56
Q

A 55 year old woman underwent a cardiovascular (CV) risk assessment with her GP using a NICE approved tool.

Which 6 of the following are significant risk factors in quantifying CV risk in the UK population?

A. Autoimmune disease
B. Blood group
C. Ear lobe creases
D. Erectile function
E. Kidney function
F. Mental illness
G. Migraine
H. Occupation
I. Post code
J. Shoe size

A

A. Autoimmune disease
D. Erectile function
E. Kidney function
F. Mental illness
G. Migraine
I. Post code

  • all are part of the Q-risk score
57
Q

An 88 year old man is seen in the clinic after an abnormal ECG is recorded prior to planned hip surgery. This shows sinus rhythm at 52 bpm with 2 ventricular ectopics, left axis deviation (-45°), first degree AV block (PR 250 ms) and left bundle branch block (QRS 140 ms).

What is the most concerning feature on his ECG?

A. Atrio-ventricular heart block
B. Axis deviation
C. Bradycardia
D. Bundle branch block
E. Ectopic beats

A
58
Q

What is the most striking abnormality in the left ventricle of older patients?

1 - mild hypertrophy
2 - mild and dilation
3 - increased stiffness (‘diastolic dysfunction’)

5 - Resting EF unchanged but blunted response to exertion

A

3 - increased stiffness (‘diastolic dysfunction’)

  • stiffness is due to fibrosis and altered Ca2+ metabolism

C. Year 3 MLA Cardiovascular Conditions/Diseases (26 decks)

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