Brainscape's Knowledge GenomeTM

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


See full index

🫀Biochemistry > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

Hyperlipidemia

A

Abnormal elevated levels of lipids/lipoproteins in blood
Chronic disease - ongoing medication
Lead to atherosclerosis

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

Exogenous lipid metabolism pathway

A

1) dietary lipids into chylomicrons in the intestine
2) chylomicrons enter circulation to peripheral tissues. Lipoprotein lipase release free FA - metabolised by muscle/adipose tissue = chylomicron remnants
3) chylomicron remanants are taken up by the liver in the formation of HDL

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

Endogenous lipid metabolism pathway

A

1) VLDL formed in the liver from triglycerides and cholestrol esters
2) triglycerides carried in VLDL are metabolised in muscle and adipose tissue by lipoprotein lipase releasing free FA = IDL formed
3) IDL is futher metabolised to LDL. Taken up by LDL receptors in tissues - liver = bile acids + secreted to intestines

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

Atherosclerosis primary causes

A

gene mutations in defective clearanve of triglycerides and LDL or excessive clearance of HDL

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

Atherosclerosis secondary causes

A 
Sedentary lifestyle - high calorie diet
Diabetes
Kidney Disease
Hypothyrodism
Obesity
Obstructive Liver Disease
Alcohol/Smoking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Hypercholesterolemia

A

Increase in cholestrol only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hypertriglyceridemia

A

Increase in triglycerides only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Combined hyperlipidemia

A

Increase in both cholestrol and triglycerides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Type 2a - familal hypercholestrolemia

A

Defect = reduction in LDL receptor
Serum abnormality = increased LDL - clear
Clinical features = Xanthelasma + Arcus senilis + Tendon Xanthomas
Treatment = statins/niacin/cholestyramine or cholestipol

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

Type 2b - familal combined hypercholestrolemia

A

Defect = reduction in LDL receptors & increased Apo B
Serum abnormality = Increased LDL and VLDL - clear
Treatment = statins/niacin/fibrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Xanthomas

A

yellow deposists of cholestrol rich material - skin lesions anywhere in body.
accumulation of lipids as large foam cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

High levels of LDL - Hypercholesterolemia symptoms

A

arcus cornea
xanthomas at achillies/elbow/knee tendons
xathelasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

High levels of TG - hypertriglycerliemia symptoms

A

xathomas

acute pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Xanthelasma

A

Yellow plaques of cholestrol deposits that occur on/ around eyelids
Can also occur in primary biliary cirrhosis and normal lipid levels
Type 2a familial hypercholesterolaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Serum lipid profile

A

total cholestrol
TG
HDL
LDL

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

Diagnosis - primary

A

Serum total cholestrol > 240mg/dL
Onset of premature CVD (<60)
Family history of CVD

17
Q

Diagnosis - secondary

A 
Fasting glucose
Liver enzymes
Creatinine
TSH
Urinary protein
18
Q

Familial Hypercholesterolemia

A

Genetic disorder
High levels of LDL from birth = early CVD
Mutations in the LDLR - normally removes LDL from circulation or ApoB - part of LDL that binds with the receptor
Heterozygous for LDLR gene = premature CVD
Homozygous = severe CVD in childhood

19
Q

Class 1

A

no LDLR synthesis

20
Q

Class II

A

no LDLR transport = not properly transported from ER to golgi for expression on cell surface

21
Q

Class III

A

no LDL or LDLR binding = LDLR does not bind LDL properly on cell surface - defect in apolipoprotein

22
Q

Class IV

A

no LDLR- LDL internalisation - LDLR bound to LDL doesn’t cluster for receptor mediated endocytosis

23
Q

Class V

A

no LDLR recycling back to cell surface

24
Q

Mutations in PCSK9 gene

A

gain in fuction of gene
enhanced activity causes LDL receptors to be broken down more quickly - reduction in number of receptors on liver cell surface. LDL not removed from blood = high blood cholestrol levels
l

25
Q

Hypertriglyceridemic Pancreatitis

A

fasting serum trigkyceride level of >150mg/dL
amylase and lipase falsely normally
causes = poorly controlled diabetes/alcohol/pancreatitis/pregnancy/ FH

26
Q

Auto digestion pancreatic injury

A

chylomicrons = large enough to occlude pancreatic capillaries -> ischemia + release of pancreatic lipase

27
Q

Hyperlipidemia treatment

A

Lifestyle changes
High LDL = statins/bile acid sequestrant + PCSK9 inhibitors
High TG = niacin/fibrates + omega 3 FA

🫀Biochemistry (2 decks)

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