Anti Dyslipidemic Flashcards
Anti-Dyslipidemic agents are drugs used to treat __________________ in the body
dysregulations in the Lipid levels
Lipids are (organic or inorganic ?) compounds that are ________ in water but _____ in organic solvents
Organic
poorly soluble
miscible
Lipids are (soluble or insoluble?) in blood
Insoluble
TRANSPORT of Lipids
Lipids are bound to _______ in blood an transported as complexes called _______
plasma proteins
LIPOPROTEINS
LIPOPROTEIN = _____ + ________
LIPIDS + APOLIPOPROTEIN
The main classes of lipoprotein includes
?????
CHYLOMICRONS.
VERY LOW-DENSITY LIPOPROTEIN (VLDL) LOW-DENSITY LIPOPROTEIN (LDL) HIGH-DENSITY LIPOPROTEIN (HDL)
Mention the apolipoproteins they have
Chylomicrons- _________
VLDL-_________
LDL-__________
HDL-__________
A1, A4, A5, B-48
B100, C, E
B100
A1,A2, E
CHYLOMICRONS
Formed ___GENOUSLY from ______
EXO
DIETARY sources
CHYLOMICRONS
Contains mainly _________
Transport them from the ____ to the ___ for ____
TRIGLYCERIDES
G.I
TISSUES; STORAGE
VLDL –
Formed ____genously in the ____
Endo
liver
VLDL –
Contains ______________
Transports its contents from the _____ to the _____ for _______
both TRIGLYCERIDE and
CHOLESTEROL
LIVER; TISSUES; STORAGE
LDL-
Formed _____GENOUSLY through ____________
ENDO
the breakdown of VLDL
LDL-
Contains _________
Transports it from the ____ to the _____ for _____
only CHOLESTEROL
LIVER
TISSUES
STORAGE
HDL
Formed ___GENOUSLY in ______
ENDO
the TISSUES
HDL
Contains _________
Transports them from _______ to ________ for _________
only CHOLESTEROL
the TISSUE; the LIVER
EXCRETION
Dyslipidemias means presence of a ___________ in the body
deranged Lipoprotein levels
DYSLIPIDEMIA
is characterized by the combination of
( low or high?) LDL-(Cholesterol or triglyceride?)
( low or high?) VLDL - (Cholesterol or triglyceride?)
( low or high?) HDL - (Cholesterol or triglyceride?)
High; Cholesterol
High; Triglyceride
Low; Cholesterol
AETIOLOGY of DYSLIPIDEMIAs
PRIMARY DISORDERS
_____________ disease
Includes
????
Inherited
TYPE I TYPE IIa TYPE IIb TYPE III TYPE IV TYPE V
AETIOLOGY of DYSLIPIDEMIAs
SECONDARY DISORDERS
Diabetes mellitus
Obesity
Alcoholism
Nephrotic syndrome Chronic renal failure Liver disease Hypothyroidism Drugs
You understand 🍻
DYSLIPIDEMIA: CLINICAL FEATURES
______ological
_______ological
____________
Dermat
Ophthalm
Gastrointestinal
DYSLIPIDEMIA: CLINICAL FEATURES
Dermatological
————-
__________
___________
Xanthomas
Xanthelasmas
Xanthomata
DYSLIPIDEMIA: CLINICAL FEATURES
Ophthalmological
_______
__________/______
Lipemia retinalis
Arcus lipoides cornea/ arcus senilis
DYSLIPIDEMIA: CLINICAL FEATURES
Gastrointestinal
________ or _______
Fatty Liver or Hepatic Steatosis
COMPLICATIONS of DYSLIPIDEMIA
State which is attributed to cholesterol and which is to triglycerides
Atherosclerosis
Angina pectoris
Myocardial infarction
cholesterol
cholesterol
cholesterol
COMPLICATIONS of DYSLIPIDEMIA
State which is attributed to cholesterol and which is to triglycerides
Ischemic cerebrovascular disease/ Stroke Peripheral vascular disease
Pancreatitis
cholesterol
triglycerides
DIAGNOSIS of DYSLIPIDEMIA
Lipid Profile:
_______
_________
_________
___________
Total Cholesterol
LDL Cholesterol
HDL Cholesterol
Triglyceride
Target cholesterol levels
Total cholesterol - less than ______mg/dL
LDL - less than ______mg/dL
HDL- _____ mg /dL or higher
Triglycerides-less than ______mg/dL
200
100
60
150
Non-Pharmacological TREATMENT of DYSLIPIDEMIA
_____ modification
________
________ restriction
Dietary
Exercise
Alcohol
Non-Pharmacological TREATMENT of DYSLIPIDEMIA
Dietary modification such as _______ , _____,——— etc
Low calories
Low saturated fats
High fiber
Anti-Dyslipidemic agents
Includes
_________
_________
_________
_________
_________
_________
STATINS
FIBRATES
NIACIN
BILE ACID RESIN EZETIMIBE
FISH OIL DERIVATIVES.
STATIN
EXAMPLES
???
Simvastatin
Lovastatin
Pravastatin
Fluvastatin
Rosuvastatin
Atovastatin
MECHANISM OF ACTION of STATIN
Inhibit the _________ of _______ in the ____
endogenous synthesis ; cholesterol; Liver
MECHANISM OF ACTION of STATIN
Bind and block ________________________ in the _____ pathway.
3-HYDROXY-3- METHYLGLUTARYL COENZYME A (HMG- COA) REDUCTASE
Cholesterol
Statins lead to reduction in _____
LDL
The rate-limiting enzyme in cholesterol synthesis is _________, which catalyzes the conversion of ________ to ________
HMG-CoA reductase
HMG-CoA to mevalonic acid.
Statins
In response to the reduced free cholesterol content within hepatocytes, synthesis of ______ is increased and their degradation is reduced.
LDLreceptors
Statins also can reduce LDLlevels by _________________ and by _______________
enhancing the removal of LDLprecursors (VLDL and IDL)
decreasing hepatic VLDL production.
Statins have a triglyceride-lowering effect
T/F
If T, how?
If F, why?
T
By decreasing hepatic VLDL production.
Statins lead to
___%-___% ↓LDL-C,
__% ↓ TG
__%-____% ↑ HDL-C
20; 50
5
5; 15
ADVERSE EFFECT of STATINS
______ pain
_____ Distress
Elevated _________
Insomnia
Muscle (Myalgia)
GI
liver enzymes
ADVERSE EFFECT of STATINS
Insomnia
________.
_________lysis
__________
Rash
Rhabdomyo
Angio-edema.
MECHANISM OF ACTION of NIACIN
It works in _______ and in the _____
In Adipose
In Liver
MECHANISM OF ACTION of NIACIN
In Adipose
Bind and block __________ in adipose tissue thereby Decreases _______________
HORMONE-SENSITIVE LIPASE
break of triglyceride into plasma Fatty acid
MECHANISM OF ACTION of NIACIN
In Liver
Inhibits the __________ of ______ , thereby Reducing _________
ESTERIFICATION of Fatty acid
Triglyceride synthesis
Niacin lead to reduction in ___________
VLDL and LDL
Niacin leads to
____-___ % ↓ TG
___-___% ↑ HDL-C
___-___% ↓ LDL-C
35–45
30–40
20–30
ADVERSE EFFECT of NIACIN
Flushing
Heart _____
________ distress
Skin _______
Palpitations
Gastrointestinal
Itching(Pruritus)
ADVERSE EFFECT of NIACIN
Flushing
Elevated ______
_______toxicity
Hyper_______
Liver enzymes
Hepato
uricemia
EXAMPLES of FIBRATES
??
Bezafibrate
Ciprofibrate
Gemfibrozil
Fenofibrate
Clofibrate
MECHANISM OF ACTION of FIBRATES
Activates _____________ which Increase __________ for _________ and _____
PEROXISOME PROLIFERATOR
ACTIVATED RECEPTOR-ALPHA (PPARα)
transcription of the genes
Lipoprotein lipase and Apo A1 and A5.
Fibrates lead to decrease ______ levels.
VLDL
____________________ (PPARα)
PEROXISOME PROLIFERATOR
ACTIVATED RECEPTOR-ALPHA
Flushing noticed after taking ______ is associated with production of ____ and is reduced by taking the dose 30 minutes after _____
NIACIN
PGD2
aspirin
Fibrates leads to
____% ↓ TG
____% ↓ LDL-C
_____% ↑ HDL-C
50
10
15
ADVERSE EFFECT of FIBRATES
Nausea, Rash
______
Muscle _______(_____)
Gallstones
Infection; Myositis
ADVERSE EFFECT of FIBRATES
__________
________uria
______________ failure
Rhabdomyolysis
Myoglobin
Acute renal
BILE ACID BINDING RESIN
List 3 examples
Cholestyramine
Colestipol
Colesevelam
MECHANISM OF ACTION of BILE ACID BINDING RESIN
It ________ bile acids in the intestine and prevent ______________
Sequesters
their reabsorption and enterohepatic recirculation
Bile acid binding resin leads to reduction in ____________
Total Cholesterol
ADVERSE EFFECT Of BILE ACID BINDING RESIN
Bloating, Constipation
Unpleasant _____
Impaired ___________
gritty taste
lipid soluble Vitamin absorption
ADVERSE EFFECT Of BILE ACID BINDING RESIN
Impaired drug absorption
_____,_____,_____
Thiazide diuretics
Warfarin
Statin
MECHANISM OF ACTION of EZETIMIBE
Bind and blocks _______ in the ______ of the small intestine
This leads to inhibition of __________
NPC1L1 transport
brush border; intestinal cholesterol absorption
Ezetimide leads to the reduction in ______
Total Cholesterol
FISH OIL DERIVATIVE Reduce __________ but increase _______
plasma triglyceride concentrations
cholesterol.
_____________ (PUFA)
n-3 polyunsaturated fatty acids
Dietary supplementation with n-3 polyunsaturated fatty acids (PUFA) improves survival in patients who have recently had a myocardial infarction.
T/F
T
Cardiovascular disease is a leading cause of morbidity and mortality in the developed countries.
T/F
T
Numerous epidemiological studies have demonstrated that cardiovascular risk increases significantly as low-density lipoprotein cholesterol (LDL-C) ______eases.
incr
Hypercholesterolaemia: A state of _____________ in the plasma.
• Dyslipidemia: a state of ______in the levels of plasma _______ and _______
elevated levels of cholesterol
abnormalities
lipids and lipoproteins.
Treatment Strategies
Lifestyle Modifications
• This has been shown to lower serum cholesterol levels, with the most notable benefits coming from ______ and ______
diet and weight loss.
Treatment Strategies
Lifestyle Modifications
Dietary strategies include reducing cholesterol intake to <_____ mg daily and reducing total fat intake to <____ % of total caloric intake.
200
20
Treatment Strategies
Lifestyle Modifications
• Inclusion of dietary soluble fibre, phytosterol esters, soy isoflavones, and nuts have all been shown to _________
reduce LDL-C
________ are the mainstay of treatment for elevated LDL-C levels
Statins
______ are the most commonly prescribed pharmacological agent used to lower LDL-C.
Statins
Cholestyramine and colestipol bind drugs like ______,_______,______, and ______ . Therefore, there is need to space drugs and resin administration by ______
digoxin, tetracycline, statins and thiazide diuretics
3-4 hours.
Examples of bile acid resins
______,________,_______
Cholestyramine, colestipol, and cholesevelam
Inhibitors of intestinal absorption of cholesterol
• Examples: ___________ and ________
Plant stanol esters and Ezetimibe
Plant stanol esters (present in food products like ________)
margarine
Plant stanol esters ___________________.
Ezetimibe reduces _______________ by inhibiting the intestinal and hepatic _______________ protein, thereby _________________
block the absorption of dietary cholesterol
dietary and biliary cholesterol absorption
Niemann-Pick C1-Like 1
lowering total cholesterol and LDL-C levels.
PCSK9 Inhibitors
• PCSK9 acts by ___________, thereby ____________.
Inhibition of PCSK9 leads to _____eased LDL receptor breakdown, thereby ___easing hepatic uptake of LDL, and (lower or higher?) serum LDL levels.
degrading LDL receptors
reducing the hepatic uptake of LDL
decr; incr
Lower
PCSK9 Inhibitors
• Examples:____________ and _________
Alirocumab and evolocumab
______________________________ (PCSK9)
Proprotein convertase subtilisin/kexin type 9
Novel Agents
• One pharmacological therapy targets ___________(CETP), which normally works to facilitate the transfer of ________ from _____ to ______ .
CETP inhibition has been shown to lead to ____eases in HDL-C and ____eases in LDL-C and lipoprotein(a) levels.
cholesterylester transfer protein
cholesteryl esters and triglycerides
HDL to lipoproteins
incr; decr
Novel Agents
• Example: __________
Anacetrapib
