Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

AP0510 Medical Biochemistry > Lipids and Cardiovascular Diseases > Flashcards

Lipids and Cardiovascular Diseases Flashcards

You may prefer our related Brainscape-certified flashcards:
USMLE® Step 1 flashcards
1
Q

Types of lipid

A
  • fatty acids (saturated or unsaturated)
  • glycerides
  • complex lipids
  • nonglycerides (sphingolipids, steroids)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Steroid class of lipids

A
  • Cholesterol
  • Cell membranes, female sex hormones, vitamin D, bile salt precursor and adrenocortical hormones
  • Linkage to CVD
  • Bile Salts
  • Important in lipid digestion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Lipoproteins

A
  • complex lipid
  • Molecular complexes found in blood plasma
  • contain: neutral lipid core of cholesterol esters and/or TAG
  • Surrounded by layer of: phospholipid, cholesterol, protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Major classes of lipoproteins

A
  • Chylomicrons: very large and very low density, transport intestine - adipose
  • VLDL: made in liver, transport lipids to tissues
  • LDL: carry cholesterol to tissues
  • HDL: good cholesterol, made in liver, scavenge excess cholesterol esters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Global atlas of CVD

A
  • CVDs account for >17 million deaths globally each year
  • correlates to 30% of all deaths worldwide
  • mortality from CVD reveals 80% occur in low-income and middle-income countries,
  • figure is expected to grow to 23.6 million by 2030
  • Ischaemic heart disease alone; 7 million deaths in 2010, 35% increase since 1990.2
  • Coronary heart disease (CHD) is largest contributor to CVD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Obesity driven Lipid based abnormalities

A
  • Imbalance in food intake, life style and genetic factors lead to Obesity
  • Obesity aggravates: dyslipidaemia, hypertension and insulin resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Healthy total cholesterol level

A
  • below 200 mg/dL (5.2 mmol/L)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Healthy LDL cholesterol

A
  • below 130 mg/dL (3.4 mmol/L)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Healthy HDL cholesterol

A
  • above 40 mg/dL (1 mmol/L) in men

- above 50 mg/dL (1.3 mmol/L) in women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Laboratory analysis

A
  • Fasting lipid profile: Total cholesterol, HDL, and triglycerides are measured
  • LDL level can be measured directly using assays or estimated using Friedewald formula
  • [LDL-chol] = [Total chol] - [HDL-chol] - ([TG]/2.2) where all concentrations are given in mmol/L
  • if calculated using all concentrations in mg/dL then the equation is [LDL-chol] = [Total chol] - [HDL-chol] - ([TG]/5)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Structure of lipoproteins

A
  • free cholesterol
  • peripheral apoprotein (A, C or E)
  • phospholipid
  • cholesterol ester
  • triglyceride
  • integral apoprotein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Apolipoprotein B (apo B)

A
  • proteincomponent of lipoproteins, complexes that transport lipids throughout the bloodstream
  • two forms of apo B: apo B-100 (made by liver) and apo B-48 (made in intestines)
  • provide structural support to lipoproteins and shield the water-repellent (hydrophobic) lipids at their centre
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Role of ApoB

A
  • Apo B-48: integral part of the structure of chylomicrons, large lipoproteins responsible for initial transport of dietary lipids from intestines to liver
  • In the liver, body repackages lipids and combines them with apo B-100 to form triglyceride-rich VLDL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Formation of LDL ApoB

A
  • In bloodstream, lipoprotein lipase (LPL) removes triglycerides from VLDL to create IDL and then, LDL
  • Lab tests for apo B typically measure only apo B-100 but are often reported as simply apo B
  • Apo B-100 concentrations tend to mirror the concentration of LDL-C
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Glucocorticoid suppressive

Hypo-aldosteronism

A
  • autosomal dominant

- mutation causes fusing of regulatory sequence of steroid 11b hydroxylase with aldosterone synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Liddle Syndrome

A
  • autosomal dominant

- activating mutant in distal convoluted tubules sodium transporter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Gordon Syndrome

A
  • autosomal recessive

- mutation leads to increased distal renal tubule chloride reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Steroid 11β-hydroxylase deficiency

A
  • autosomal recessive

- leads to plasma 11-deoxycortisol and 11-deoxycorticosterone increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Steroid 17α- hydroxylase deficiency

A
  • autosomal recessive

- leads to plasma 11-deoxycortisol and 11-corticosterone increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Xanthelasmas

A
  • type of xanthoma; raised, yellowish macules that typically appear around the medial canthus, can extend to the eyelids or skin immediately below the eye
  • occur in patients with FH, familial defective apoB100, or
    dysbetalipoproteinemia
  • occasionally occur in patients with normal cholesterol levels
  • regress w/cholesterol lowering and may be treated with cholesterol-lowering drugs
21
Q

Dysbetalipoproteinemia

A
  • rare familial dyslipidemia characterized by approx. equally elevated serum cholesterol and triglyceride levels due to accumulated remnant lipoproteins in apolipoprotein E2/E2 homozygotes
  • associated with increased risk for premature CVD
22
Q

Lipemia retinalis

A
  • lipemic blood causes opalescence of retinal arterioles
  • can be observed during funduscopic examination
  • typically seen only when the triglyceride levels are 22.6 mmol/L (2000 mg/dL) or higher
23
Q

Tendon xanthomas

A
  • nodular deposits of cholesterol that accumulate in tissue macrophages in the Achilles and other tendons, including the extensor tendons in the hands, knees, and elbows
  • often present in patients with FH or familial defective apoB100 and sometimes in those with dysbetalipoproteinemia
24
Q

Tuberous or tuboeruptive xanthomas

A
  • Develop in areas such as the elbows and knees
  • range from pea-sized to lemon-sized and can be seen in dysbetalipoproteinemia and FH
  • Palmar xanthomas: found in the palmar and digital creases of the hands. Almost pathognomonic for high plasma levels of β-VLDL and dysbetalipoproteinemia.
  • caused by accumulation of triglyceride in dermal histiocytes and occur when the plasma triglyceride level is 11.3 to 22.6 mmol/L (1000 to 2000 mg/dL) or higher
  • can disappear rapidly with lowering of the plasma triglyceride concentration
25
Q

Thrombosis

A
  • healthy human heart
  • plaque with fibrous cap
  • cap ruptures
  • blood clot forms, blocking artery
  • dead heart tissue qt blockage site
  • coronary thrombosis: formation of a blood clot inside blood vessel of the heart, restrict blood flow within the heart, leading to heart tissue damage, or heart attack
26
Q

Obesity-Induced Changes in Adipose Tissue and Impact on CVD

A
  • Functional adipose tissue, found in lean organisms, express anti-inflammatory adipokines that protect against CVD
  • excess adipose tissue expansion promotes dysfunction, leading to the expression of proinflammatory adipokines that promote CVD
27
Q

Insulin resistance

A
  • adipokine imbalance can affect function of metabolically important tissues and the microvasculature, promoting insulin resistance and indirectly contributing to CVD
28
Q

Wider Impact of elevated Lipid Levels

A
  • CVD
  • sensory neuropathy
  • erectile dysfunction
  • renal impairment
  • cognition
29
Q

Common Lipid Disorders that Lead to Atherosclerosis

A
  • Dyslipidemia: abnormal lipoprotein levels (LDL and HDL) in association with an increased risk of CVD
  • Hyperlipidemia: elevated blood lipid levels (total cholesterol, LDL, triglycerides)
  • Hypercholesterolemia: elevated total cholesterol> 200 mg/dL
  • Hypertriglyceridemia: elevated triglyceride levels
  • Hyperlipoproteinemia: elevated levels of a certain lipoprotein
30
Q

Acute Myocardial Infarction (AMI)

A
  • If diagnosed quickly and the patient sent to a CCU then appropriate care can be initiated
  • trouble its too expensive for everyone who comes in with chest pain, since it could be simply heart-burn
  • WHO classification relies on any 2 of the following:-
  • Severe chest pain that lasts for more than 30 mins
  • characteristic ECG changes
  • and finally a characteristic rise and fall in cardiac enzymes, now changes in Cardiac Markers
31
Q

Aspartate Transaminase

A
  • Poor clinical specificity
  • Ref. range: male <56 IU/L female <45 IU/L
  • detect an increase in AST it could be from the heart, liver or skeletal muscle, and although clinical symptoms should help determine the source, we can’t be 100% sure
32
Q

Factors into increased AST

A
  • haemolysis: RBC’s have slightly more AST, levels are only raised slightly
  • post partum, levels can be increased due to trauma of birth itself
  • cholestasis
  • liver metastases
  • post op
  • haemolytic disease
  • viral hepatitis
  • toxic liver necrosis
  • circulatory failure
33
Q

Lactate dehydrogenase

A
  • Ref. range: 90-230 IU/L
  • Increased LD: viral hepatitis, malignancy, pulmonary embolism, shock
    leukaemia, haemolysed samples, AMI
34
Q

Creatine kinase

A
  • very important for energy storage and production, muscle and brain have very high levels
  • catalyses reversible transfer of phosphate between ATP and creatine to produce creatine phosphate and ADP
  • Ref. Range: males 40-165 IU/L, females 40-150 IU/L
35
Q

Factors into increased CK

A
  • Haemolysed sample
  • IM injections
  • hypothyroidism
  • neonates
  • post -partum
  • muscular dystropy
  • surgery/trauma
  • AMI
36
Q

Measuring CK-MB

A
  • Immuno assay
  • Immobilising through binding only the M subunit
  • Eliminate CK containing B subunit
  • Differential binding of the antibody with the B subunit
    this enables binding only with the B subunit of CK enzyme
  • results in only measuring the cardiac specific CK-MB isoform
37
Q

Relative index of CK-MB and AMI protocol

A
  • Relative Index = CK-MB Mass / Total CK x100
  • If total CK is high and CK-MB is <5% of total = not cardiac
  • If total CK is high and CK-MB is >15% = cardiac
38
Q

New markers for AMI

A
  • Myoglobin (small, released at 30mins)
  • CK-MB isoforms (lysine – not hydrolysed)
  • Troponins
39
Q

Tropomyosin

A
  • 2 strands of a thin protein which are wrapped around each other like a helix to give them strength
  • Along the chains are globular proteins called actin
40
Q

Troponin

A
  • along the thin tropomyosin filaments is a cluster of 3 proteins
  • first is troponin-I or inhibitor complex
  • This is pulled out of the way by troponin-C in the presence of calcium (this is increased when a nerve impulse to contract is received)
  • With inhibitor out of the way the T protein (which is the 3rd in the complex) can interact with the other muscle protein fibres
41
Q

Myosin

A
  • Each bundle is made up of a long protein strand with a sticky head
  • There are hundreds or thousands of these in each myosin bundle
  • troponin-T can interact with these stick heads and forms a complex
42
Q

Troponin and myosin interaction

A
  • signal to contract is received, the calcium levels go up and allows the troponin-T to alter its structure
  • causes it to stretch and interact with another myosin head further along the filament
  • ATP used in this process is sufficient to pull the troponin back to its original position and also pulls the mysoin fibre with it
43
Q

Troponins as cardiac markers

A
  • Troponin-C: same in all muscle types, not specific
  • cTnT: levels rise within 3-4 hrs, peak at 10-12 hrs, 10-14 days to return to normal, Some renal interference
  • cTnI: considered more cardiac specific, levels rise within 3-6 hour, peak at 14-20 hours, return to normal after 5-6 days
44
Q

Diet (management of CVD risk)

A
  • Professional advice to compose suitable diet
  • Aims: weight reduction, reducing blood pressure, appropriate lipid and glycaemic control
  • Increase intake of fruit and veg, wholegrain cereals and bread, lean meat and fish (omega-3 oils)
  • Replace saturated fats (animal fats) with complex carbs, monosaturated and polyunsaturated fats (vegetable and seafood)
45
Q

Increase physical exercise (management of CVD risk)

A
  • Should be encouraged in ALL age groups and all patients
  • Healthy individuals: 30-45 minutes, 4-5 times a week at 60-75% of average maximum heart rate
  • High risk/establish CVD patients: exercise regime based on comprehensive clinical assessment and judgement
46
Q

Blood pressure (management of CVD risk)

A
  • Risk of CVD increases as BP rises from normal
  • Decision to treat depends on assessment of total cardiovascular risk, evidence of target organ damage as well as actual BP
47
Q

Behavioural risk factors (management of CVD risk)

A
  • Diet, smoking, sedentary lifestyle

- Very difficult to alter; socioeconomic factors, stressful lifestyles, lack of social support, negative emotions

48
Q

Expert consultations (management of CVD risk)

A
  • Ensure patients understand relationships between behaviour, health and disease
  • Gain commitments to behavioural change
  • Involve patients in identifying and selecting risk factors to change
  • Design of lifestyle modification plans; Diet, exercise
  • Monitor progress through follow ups
  • Involve appropriate healthcare staff wherever possible

AP0510 Medical Biochemistry (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions