Lipid series 2.pptx

PABITRA THAPA
SR. PRODUCT MANAGER

LIPIDS
• Lipids are hydrophobic substances made mainly of carbon,
hydrogen and oxygen atoms.
PABITRA THAPA, PRODUCT
MANAGER

Sources of Lipids
1. Diet
2. Synthesis
• Lipid Digestion
1 Mouth and Stomach
• Lipids (Fats) present in our food is hydrolysed in low
degree by lingual lipase and gastric lipase.
2 Intestine
On reaching lipids contents from Stomach to intestine, these
lipids content stimulates small intestinal mucosal cell to
release hormone CHOLECYSTOKININ.
CHOLECYSTOKININ stimulates gall bladderand
pancrease to release bile and digestive enzymes
respectively
• So Lipds are emulsifed and absorbed by small intestinal cell.
MANAGER

MANAGER

Still, absorbed emulsified lipid is not transported.
So this lipid combine with proteins in in the
intestinal cell to form Liporoteins and cirulated via
Lymphatic system and blood.
There are four major classes of circulating lipoproteins
1. Chylomicrons,
2. very low-density lipoproteins (VLDL),
3. low-density lipoproteins (LDL),
4. Intermediate-density lipoproteins (IDL) and high-density
lipoproteins (HDL)
MANAGER

There are 4 main types of lipoprotein
1. Chylomicrons: Formed in intestinal mucosal cell
(Rich in TGS)forms in GIT (intestinal Lining)
from dietary TG and secreted into the
lymphatic circulation.
These lipoproteins move into the blood
stream where they got hydrolyzed by
endothelial lipoprotein lipase which
hydrolyzes the triglyceride into glycerol and non-
esterified fatty acids.
MANAGER

2. VLDL (Rich in Colesterol & TGs)
Formed in liver
From Blood, chylomicron remnants are
absorbed in the liverand packaged with
cholesterol,cholesteryl esters and ApoB100
to form VLDL.
MANAGER

3. IDL( TGs and Cholesterol)
After the release of VLDL into the blood stream it will be
converted into IDLby the action of lipoprotein lipase and
hepatic lipase.
4. LDL (Cholesterol)
Again , hydrolysis by hepatic lipase, IDL will be converted to
LDL.
LDL carry cholesterol to all parts of the body.
MANAGER

LDL (BAD LIPIDS ):
Low density lipoproteins (LDL) are considered “bad”
cholesterol.
While they carry needed cholesterol to all parts of the body,
too much LDL in the system can lead to coronary artery
disease, due to the buildup of LDL deposits in the artery walls
 Together with other substances, it can form plaque, a thick,
hard deposit that can narrow the arteries and make them less
flexible.
 This condition is known as atherosclerosis. If a clot forms and
blocks a narrowed artery, heart attack or stroke can result
MANAGER

• Cholesterol is lost from cells
in peripheral tissues by transfer to another
type of circulating lipoprotein (HDL) in the
blood and is then returned to the liver, where
it is metabolized to bile acids and salts.
MANAGER

HDL (GOOD LIPIDS):
High-density lipoproteins – collect cholesterol
particles as they travel through blood vessels and
deposits them in the liver where they are transferred
to bile acids and disposed off.
A higher HDL score is desirable and will improve
overall cholesterol score.
MANAGER

TOTAL
CHOLESTEROL
• Desirable: <200 mg/dL
• Borderline high: 200-239 mg/dL
• High: > or =240 mg/dL
TRIGLYCERIDES
• Normal: <150 mg/dL
• High: 200-499 mg/dL
• Very high: > or =500 mg/dL
•
HDL CHOLESTEROL
Males
• > or =40 mg/dL
Females
• > or =50 mg/dL
LDL CHOLESTEROL
• Desirable: <100 mg/dL
• Above desirable: 100-129 mg/dL
• High: 160-189 mg/dL
• Very high: > or =190 mg/dL
MANAGER

Hyperlipidemia classification
• Hyperlipidemia general can be classified to:
Primary:
It is also called familial due to a genetic defect,
1. It may be Monogenic: a single gene defect or
2. Polygenic: multiple gene defects.
MANAGER

Secondary:
• it is acquired because it is caused by another
disorder like
• diabetes, nephritic syndrome, chronic alcoholism,
hypothyroidism and with use of drugs like
corticosteroids, beta blockers and oral
contraceptives.
• Secondary hyperlipidemia together with significant
hypertriglyceridemia can cause pancreatitis.
MANAGER

Complications of Hyperlipidemia
• Atherosclerosis: Hyperlipidemia is the
most important risk factor for
atherosclerosis, which is the major cause
of cardiovascular disease.
• Atherosclerosisis a pathologic process
characterized by the accumulation of
lipids, cholesterol and calcium and the
development of fibrous plaques with in
the walls of large and medium arteries
MANAGER

Fatty deposits build up in blood vessel walls and. resulting in
narrowing of the the arteries that supply blood to the myocardium,
and results in limiting blood flow and insufficient amounts of
oxygen to meet the needs of the heart
• The resulting condition, called atherosclerosis
often leads to eventual blockage of the coronary
arteries and a “heart attack”.
MANAGER

• Eventually, the reduced blood flow may cause chest
pain (angina), shortness of breath, or other coronary
artery disease signs and symptoms. A complete
blockage can cause a heart attack.
• Because coronary artery disease often develops over
decades, one might not notice a problem until you
have a significant blockage or a heart attack
MANAGER

Myocardial Infarction (MI):
• MI is a condition which occurs when blood and
oxygen supplies are partially or completely blocked
from flowing in one or more cardiac arteries,
resulting in damage or death of heart cells. The
occlusion may be due to ruptured atherosclerotic
plaque.
• The studies show that about one-fourth of survivors
of myocardial infarction were hyperlipidemic
MANAGER

Ischemic stroke:
• Strokes occur due to blockage of an artery by a blood
clot or a piece of atherosclerotic plaque that breaks
loose in a small vessel within the brain.
• Many clinical trials revealed that lowering of low-
density lipoprotein(LDL) and total cholesterol by
15% significantly reduced the risk of the first stroke
MANAGER

Classification of drugs
1. HMG-CoA reductase inhibitors:
Atorvastatin, Simvastatin,Rosuvastatin, Pravastatin,
Fluvastatin
2. Bile acid Sequestrants (resin):
Cholestyramine, Colestipol
3. Activate Lipoprotein Lipase (Fibric acid derivatives):
Clofibrate, Gemfibrozil,
Fenofibrate
4. Inhibit lipolysis & triglyceride synthesis: Nicotinic
acid
5. Others: Ezetimibe,
MANAGER

Mixed dyslipidemia
• Mixed dyslipidemia is defined as elevations in
LDL cholesterol and triglyceride (TG) levels
that are often accompanied by low levels of
HDL cholesterol.
MANAGER

MOA
Significantly decrease plasma triglycerides
Moderate decrease in LDL cholesterol
Increase in HDL cholesterol concentrations
Decrease in VLDL production
Increase hepatic excretion of cholesterol
MANAGER

Triglycerides
• Stimulation of lipoprotein lipolysis.
• Increase hepatic fatty acid (FA) uptake and
• reduction of hepatic triglyceride production.
• enhance the production of fatty acid transport protein and
acyl-CoA synthetase, which contribute to the increase
uptake of fatty acid by the liver and
• as a result in a lower availability of fatty acids for
triglyceride production
MANAGER

Dose of Fenofibrate
• Fenofibrate capsules are administered orally once daily with or without food.
• Dose adjustments are made at 4 to 8-week intervals based on
the individual patient response.
• Hypertriglyceridemia (type IV or V)
– 40 to 160 mg daily
• Hypercholesterolemia
• Mixed dyslipidemia
MANAGER

Precautions
• Patients with hepatic impairment should avoid the
use of fenofibrate. No dose adjustment is necessary
for patients with renal impairment if creatinine
clearance is above 80 mL/min
• Fenofibrate is contraindicated if creatinine clearance
is under 30mL/min or if the patient has severe renal
dysfunction.
MANAGER

CI
• Fenofibrate is contraindicated for patients
with a history of hypersensitivity to
fenofibrate, liver disease, severe renal
dysfunction, preexisting gallbladder disease,
or breastfeeding.
MANAGER

Fenofibrate Market size
• Yearly: Around 4.5 crore
• Major 3 brand
• TGR (Intas) : 2.3 crore
• Fenocard (Quest): 1.3 crore
• LIPICARD(USV): 0.8 crore
• Fenolip (CIPLA):
• Triglide (Grace):
MANAGER

KNOW
• Know Prescriber
• Know Counters selling Fenofibrate
MANAGER

PROMOTION
• Promote Doctors
• Promote to Stockiest
• Promote – Pharmacy
Community Pharmacy
Hospital Pharmacist
POB
MANAGER

• Sampling
• Promotional Out Put
MANAGER

Review
• Feed Back
• Stockiest feed back
• Stockist staff
• Does they know about Trichek
• Similar brand
• Trichek strength
MANAGER

• STROKE
–NEUROLOGIST
»NEUROSURGEN
MANAGER

FAST
• Face(Facial Weakness) – has their face fallen on one
side? Can they smile? Has their mouth or eye drooped?
• Arms Weakness – can they raise both their arms and
keep them there?
• Speech Problems– is their speech slurred? If they
notice any of these symptoms it is:
• Time – time to call AND GO HOSPITAL if you see
ANY of these signs
MANAGER

STROKE
• Stroke refers to any damage to the brain or spinal cord
caused by an abnormality of the blood supply.
• The terms STROKE is typically used when symptoms
begin abruptly
• WHO:- Clinical syndrome consisting of rapidly
developing clinical signs of focal disturbances of
cerebral function, lasting more than 24 h or leading to
death with no apparent cause other than that of vascular
origin
MANAGER

• Infarction: Permanent injury
• The brain requires 75 to 100 mg of glucose each minute.
• Brain measures only 2% of adult body weight but uses approx.
20% of the cardiac output
MANAGER

Types of brain Damage in Stroke
• There are two major categories of brain
damage in stroke patients.
1. ISCHEMIA: Which is lack of blood flow
depriving brain tissue from energy and
oxygen
1. HEMORRHAGE: Which is the release of
blood into the brain and into the extravascular
spaces within the cranium.
MANAGER

Ischemia
Further subdivided into 3 different mechanisms
1. -Thrombosis
2. -Embolism
3. -decreased systemic perfusion
MANAGER

1. Thrombosis
• Refers to an obstruction of blood flow due to a
localised occlusive process within one or more
blood vessels.
• The lumen of vessel is narrowed or occluded
• The main cause is atherosclerosis
MANAGER

2. EMBOLISM
Material formed else where within vascular
system lodges in an artery and blocks the flow
Blockage can be transient or may persist for
hours or days.
MANAGER

Cardiac sources of embolism:
• Include from heart valves and clots or tumors within the
atrial or ventricular cavities
• Artery-to-artery emboli.
Are composed of clots, platelet clumps, or fragments of
plagues that break off from the proximal vessels
Pradocical embolism: clots originating in systemic veins
travel to the brain
Ocassionally air, fat, particulate matter from injected drugs,
bacteria, foreign bodies, and tumor cells enter the vascular
system and embolize to brain arteries.
MANAGER

3. Decreased Systemic Perfusion
Diminished flow to brain tissue is caused by low
systemic pressure.
The most common causes are
1. Cardiac pump failure: most often due to
myocardial infarction or arrythmia
2. Systemic hypotension: due to blood loss or
hypovolemia
MANAGER

A subarachnoid hemorrhage(SAH), sometimes known as a ‘bleed on the brain’, occurs
when bleeding occurs in the subarachnoid space.
The subarachnoid space lies beneath a layer of one of the brain’s coverings known as the
meninges.
The most common cause of a subarachnoid hemorrhage is the rupture of an aneurysm.
An aneurysm occurs when the walls of blood vessels become weakened and the blood vessel dilates.
• Bleeding usually results from the rupture of an abnormal bulge in a blood
vessel (aneurysm) in our brain.
Risk factors for developing aneurysms in the brain include smoking and high blood pressure
(hypertension)
• Untreated, a subarachnoid hemorrhage can lead to permanent brain damage or
death.
MANAGER

STROKE
MANAGER

Subarachnoid Haemorrhage
MANAGER

Hepatic Cholesterol
Metabolism
MANAGER

• All STATINS are
• (3-hydroxy-3-methyl-glutaryl-coenzyme A
reductase) INHIBITOR
MANAGER

• STATIN THERAPY
• An established key component of secondary
prevention after ischemic stroke
• High-intensity statins have been explicitly
recommended for atherosclerotic cardiovascular
disease, including ischemic stroke
• According to the British NICE guideline,11 high-
intensity statin use was defined as atorvastatin ≥20
mg/day, rosuvastatin ≥10 mg/day, and simvastatin 80
mg/day, medium-intensity as atorvastatin 10 mg,
fluvastatin 80 mg, rosuvastatin 5 mg, simvastatin 20
and 40 mg,
MANAGER

BENEFITS OF STATIN THERAPY IN STROKE
Statin pretreatment increases cerebral blood flow and reduces
cerebral infarction size during cerebral ischemia
Because embolic stroke is less associated with cholesterol levels,
statin therapy is less effective in patients with embolic stroke.
In a SPARCL trial, compared with placebo controls, the high-intensity statin
(atorvastatin 80 mg) initiated after a stroke or transient ischemic attack
(TIA) resulted in a 16% reduction of nonfatal and fatal stroke and a 20%
reduction of major cardiovascular events after 5-year follow-up
Statins exert neuroprotective, microvascular, and anti-
inflammatory beneficial effects
MANAGER

Lipid series 2.pptx

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Lipid series 2.pptx