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HLB > Dyslipidaemia > Flashcards

Dyslipidaemia Flashcards

1
Q

Name? Is?

A
  • white circular line around the cornea
    arcus senilis
    corneal arcus
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2
Q

Corneal Arcus is present in

A

> 50% age 50

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3
Q

Corneal Arcus is a sign of dyslipidaemia in patients aged

A

<45 years old

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4
Q

Cholesterol (3):

  • synthesised by
  • especially
  • is an integral part of
A
  • synthesised by all animal cells
  • especially by the liver
  • integral part of the cell membranes
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5
Q

Cholesterol functional group is

A

OH
alcohol

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6
Q

Cholesterol is a member of the steroid class of molecules.

True or False?

A

True

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7
Q

What type of relationship between atherosclerotic disease and cholesterol levels?

A

Linear relationship

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8
Q

Triglyceride structure:

A
  • glycerol backbone
  • three fatty acids
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9
Q

Lipoproteins are miscible with water.

True or False?

A

False
Fats are immiscible with water

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10
Q

Lipoproteins have varying quantities of (3):

A
  • cholesterol
  • triglyceride
  • apolipoproteins
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11
Q

Fats are carried in the blood as a part of

A

lipoprotein molecules

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12
Q

Lipoprotein

A
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13
Q

Core of lipoprotein:

A
  • cholesterol (esters)
  • triglyceride
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14
Q

Surface of the lipoprotein:

A
  • cholesterol (free)
  • apolipoproteins
  • phospholipid
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15
Q

VLDL

A

very low density lipoproteins

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16
Q

Relationship between the size and density of a lipoprotein?

A

The larger a lipoprotein the lower the density

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17
Q

Which type of lipoproteins are of the lowest density and the largest size?

A

chylomicrons

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18
Q

Lipoprotein subtypes

A
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19
Q

Basic cholesterol pathway ***

A
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20
Q

What step of cholesterol synthesis is targeted most by drugs?

A
  • rate limiting step
  • HMG-CoA Reductase
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21
Q

Exogenous Pathway for lipoproteins: Label diagram and give a description:

A
  • gut to liver (fat transport)
  • dietary fats transported from the gut in
    chylomicrons
  • triglyceride component broken down the
    by LIPOPROTEIN LIPASE in capillary
    endothelium
  • remnants transported to the liver
  • liver secretes bile acids and some
    cholesterol into the gut
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22
Q

Endogenous pathway for lipoproteins: Label diagram and give a description:

A
  • liver to peripheral tissues
  • Liver produces VLDL and LDL
  • Triglyceride component of VLDL broken
    down by Lipoprotein Lipase in the
    endothelium
  • IDL transported to the liver and converted
    to LDL
  • LDL binds to LDL receptors on peripheral
    tissues
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23
Q

Reverse Pathway for lipoproteins: Label diagram and give a description:

A
  • peripheral tissues to liver
  • some free cholesterol in tissues is taken up
    into HDL
  • HDL is transported to the liver
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24
Q

Ideal Lipid Profile:

A
  • low LDL
  • high HDL
  • low level of total lipoprotein/ HDL
  • low triglyceride level
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25
Q

Typical Reference Ranges for Lipids:

A
  • total cholesterol <5mmol/L
  • LDL cholesterol <3mmol/L
  • HDL cholesterol > 1.5 mmol/L
  • Total/HDL ratio <3.5
  • Triglyceride 0.5-2.0 mmol/L
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26
Q

Causes of Secondary Dyslipidaemia:

A
  • diabetes mellitus
  • hypothyroidism
  • chronic kidney disease
  • chronic liver disease
  • obesity
  • smoking
  • medications: thiazide diuretics,
    bendoflumethiazide
  • excess alcohol (increased triglyceride
    levels)
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27
Q

Primary Dyslipidaemia:

A
  • abnormal lipoprotein structure
  • abnormal lipoprotein receptors

NOT DUE TO INCREASED INTAKE OR SYNTHESIS

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28
Q

Excess alcohol consumption increases what molecule levels resulting in dyslipidaemia?

A

triglyceride

29
Q

4 types of lipoproteins and description:

A
  • Chylomicron: deliver triglycerides and
    cholesterol from the intestines to the liver
  • VLDL: deliver triglycerides from the liver to
    the tissues
  • LDL: deliver cholesterol from the liver to
    the tissues (bad cholesterol)
  • HDL: deliver cholesterol from the tissues to
    the liver
30
Q

Fredickson Classification table

A
31
Q

Familial Hypercholesterolaemia Type IIa:
- due to
- dominant or recessive?
- causes?
- what % of population?
- consider diagnosis if:

A
  • due to specific mutations that lead to the
    absence/low levels of LDL receptors
  • autosomal dominant
  • causes severe atherosclerosis and may see
    IHD in young adults especially men
  • 0.5% of the population
  • very high LDL cholesterol (>5.ommol/L,
    even at birth)
  • consider diagnosis if total cholesterol
    >7.5mmol/L
  • triglyceride levels near normal
32
Q

Familial Combined Hyperlipidaemia Type IIb:
- mutations
- dominant/ recessive
- commonly involves
- affects what % of the population
- lipid profile
- commonly associated with
- accounts for what % of premature IHD
cases

A
  • polygenetic condition
  • autosomal dominant
  • mostly involve overproduction of
    apolipoprotein B-100***
  • affects 10% of the population
  • moderately high levels of cholesterol and
    triglycerides
  • LDL, VLDL and triglycerides are all elevated
  • insulin resistance and obesity (metabolic
    syndrome)
  • accounts for 20% of premature IHD cases
33
Q

Familial Hypertriglyceridaemia Type IV:
- mutation
- affects what % of the population
- lipid profile
- associated with
- risk of
- association with IHD

A
  • multiple genetic defects, polygenic
  • 1% of the population
  • elevated triglycerides (>5.0mmol/L),
    relatively normal cholesterol, HDL often
    low
  • insulin resistance and obesity (metabolic
    syndrome)
  • risk of acute pancreatitis (if TG level >10),
    due to pancreatic capillary obstruction by
    lipoprotein accumulation
  • not strongly associated with IHD
34
Q

Familial Hyperchylomicronaemia Type I:

  • due to
  • dominant or recessive
  • lipid profile
  • key feature
  • risk
A
  • due to a deficiency of lipoprotein lipase
  • autosomal recessive
  • very high triglycerides, normal cholesterol
  • spun blood is creamy ***
  • pancreatitis more likely than IHD
35
Q

Familial dysbetalipoproteinemia Type III:

  • due to
  • dominant or recessive
  • hence
  • hence
  • lipid profile
  • increased risk of
  • clinical sign
A
  • due to a deficiency of Apolipoprotein E
  • autosomal recessive
  • poor lipoprotein clearance by the liver
  • chylomicrons and IDK remain in blood
  • modest elevations of cholesterol and
    triglycerides
  • increased risk of IHD
  • palmar xanthomas
36
Q

If a patient has very high LDL cholesterol (8mmol/L) and total cholesterol 10mmol/L and triglyceride levels are near normal, which type of dyslipidaemia?

A

Familial Hypercholesterolaemia Type IIa

37
Q

A patient has familial hypertriglyceridaemia type IV. What is the main risk with this condition, when and why would this risk occur?

A
  • risk of acute pancreatitis
  • occurs if triglyceride levels >10mmol/L
  • accumulation of lipoproteins in pancreatic
    capillaries leads to obstruction
38
Q

what type of hyperlipidaemia to consider when a patient has palmar xanthomas?

A

type III
dysbetalipoproteinemia

39
Q

Xanthomas =

A

lipid deposits in the skin
generally eyes

40
Q

What clinical sign is this?

A

Xanthesmata
Lipid deposits around the eyes
Usually lipid laden macrophages

41
Q

Tendon xanthomas

A

lipid deposits
attached to extensor surface tendons
eg: achilles tendon

42
Q

what clinical sign is this?

A

tendon xanthomas

43
Q

What clinical sign is this? Specific to which type of dyslipidaemia?

A

palmar xanthomas
lipid deposits in the skin creases of the hands
specific to familial dysbetalipoproteinemia

44
Q

What clinical sign is this? Where is it seen? Patients complain of? Condition?

A
  • eruptive xanthomas
  • reddish bumps that appear suddenly on
    elbows, forearms, trunk, legs
  • seen in severe hypertriglyceridaemia
45
Q

Core Drug: Atorvastatin:
- type of drug
- used for
- mechanism
- hence (4)

A
  • statins
  • first line for most patients with elevated
    cholesterol
  • inhibits HMG-CoA Reductase ***
  • reduces cholesterol production by the liver
  • lowers LDL, total cholesterol and
    triglyceride levels
  • increases HDL levels
46
Q

Core Drug: Simvastatin:
- type of drug
- used for
- mechanism
- hence (4)

A
  • statins
  • first line for most patients with elevated
    cholesterol
  • inhibits HMG-CoA Reductase ***
  • reduces cholesterol production by the liver
  • lowers LDL, total cholesterol and
    triglyceride levels
  • increases HDL levels
47
Q

Management of hyperlipidaemia:

A
  • lifestyle
  • statins
48
Q

Management of hyperlipidaemia: Lifestyle:

A
  • aerobic exercise
  • smoking cessation
  • alcohol moderation
  • weight loss for obese patients
  • diet: portion control, limit carbs, oily fish
    (omega 3 fatty acids)
49
Q

Why do we treat hyperlipidaemia with statins?

A
  • to prevent development/progression of
    atherosclerosis
  • reduces all cause mortality (reduction in
    death from established arterial disease
    patients hence wont take drug and die
    from a side effect of statin)
50
Q

Statins work so well because

A
  • reduces LDL, increases HDL
  • less inflammation
  • alters plaque components
51
Q

Statins reduce all cause mortality in a wide range of patients:

A
  • MI or stroke
  • CABG (coronary artery bypass grafting)
  • PCI (percutaneous coronary intervention)
52
Q

Do we use statins in patients with hyperlipidaemia who have never had a vascular event?

A

Yes
Primary prevention

53
Q

Statins for primary prevention advantages and disadvantages

A

adv: reduces risk of adverse events in higher
risk patients
disadv: medicating well patients

side effects: myalgia (muscle pains) ***
Rhabdomyolysis (dangerous
muscle breakdown)
Arthralgia (joint pains)
Liver dysfunction

54
Q

Statins side effects:

A
  • myalgia (muscle pains)
  • Rhabdomyolysis (dangerous muscle
    breakdown)
  • Arthralgia (joint pains)
  • Liver dysfunction
55
Q

What is the risk assessment tool used for hyperlipidaemia/ cardiovascular?

A

Q-risk

based on multivariate analysis from the Framingham Heart Study

56
Q

***NICE: statins for primary prevention:

A
  • if 10 year risk of cardiovascular disease >
    10%
  • Q-risk score
  • check lipids after 3 months of statins
  • aim for LDL reduction of >40% on statins
  • ***no other drugs are reccomended for
    primary prevention based on estimated
    risk
57
Q

First line drugs for patients with very high triglyceride levels?

A

Fibrates

58
Q

Core Drug: Bezafibrate:
- used
- mechanism
- hence
- side effects

A
  • first line for patients with very high
    triglyceride levels
  • activate lipoprotein lipase (endothelium),
    strips triglyceride out of chylomicrons and
    VLDL
  • lower triglyceride, LDL
  • increases HDL
  • side effects: myalgia/rhabdomyolysis, GI
    disturbances
59
Q

Is bezafibrate more potent than atorvastatin?

A

No
atorvastatin is more potent

60
Q

Bile salt sequestrants:

A
  • cholestryamine
  • absorbs bile salts that are used to absorb
    lipids and are then lost in stool
  • prevents re-uptake of bile salts in the gut
  • reduces fat absorption
  • cholesterol diverted to bile salt production
    in the liver
  • mild effect only
  • reduces LDL but increases triglycerides
  • side effects: GI disturbances
61
Q

Is cholestyramine effective?

A

Mildly

62
Q

Core Drug: Ezetimibe:
- mechanism
- hence
- lipid profile
- effective?
- commonly used
- side effects

A
  • selectively inhibits the absorption of
    cholesterol by the small intestine
  • does not alter the absorption of fat soluble
    vitamins
  • only lowers LDL
  • mild effect
  • commonly used as an add on to statins
  • side effects: GI disturbances
63
Q

is cholestyramine more selective than ezetimibe?

A

no
ezetimibe more selective

64
Q

When is ezetimibe used alone?

A

Rarely
if a patient really cant tolerate statins

65
Q

Omega-3 fatty acids and hyperlipidaemia:
- how
- does what
- side effects

A
  • atlantic salmon, tuna, anchovies
  • tablets
  • reduce VLDL synthesis by the liver
  • reduce triglyceride > cholesterol
  • side effects: GI disturbances
66
Q

Niacin=nicotonic acid= vitamin B3 and hyperlipidaemia:

  • how
  • does what
  • used for
  • side effect
A
  • inhibits lipase enzymes in adipose tissues
  • mild reduction in LDL/TG, marked increase
    in HDL
  • used for patients with very high Lp-a levels
  • side effect: facial flushing
67
Q

Evolocumab:

  • mechanism
  • used for
  • side effects
A
  • PCSK9 inhibitor (monoclonal antibody)
  • PCSK9 is a circulating enzyme which binds
    to the LDL receptor and reduces LDL
    clearance
  • hence drug inhibits enzyme so increases
    LDL clearance hence reducing LDL levels,
    and triglyceride levels also increases HDL
    levels
  • very powerful, expensive and used for
    familial hypercholesterolemia and patients
    who fail to reach target goals on statins
    alone
  • side effects: cough/flu-like symptoms
68
Q

why do PCSK9 inhibitors produce side effects like cough/flu?

A
  • all drugs of this class are monoclonal
    antibodies
  • cough and flu like symptoms are partly due
    to antibodies produced

HLB (49 decks)

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