Hyperlipidemia is a common disorder caused by abnormalities in lipid metabolism or transport. It results in high levels of lipids like cholesterol and triglycerides in the blood. Hyperlipidemia is classified based on the abnormal lipid levels and is primarily treated through lifestyle changes and medications that lower lipid levels. Common drug classes used to treat hyperlipidemia work by inhibiting cholesterol synthesis, breaking down fats, or blocking lipid absorption.
Hypolipidemic agents, also known as cholesterol-lowering drugs or antihyperlipidemic agents, are a diverse group of pharmaceuticals that are used in the treatment of high levels of fats (lipids), such as cholesterol, in the blood (hyperlipidemia). They are also called lipid-lowering drugs.
Hypolipidemic agents, also known as cholesterol-lowering drugs or antihyperlipidemic agents, are a diverse group of pharmaceuticals that are used in the treatment of high levels of fats (lipids), such as cholesterol, in the blood (hyperlipidemia). They are also called lipid-lowering drugs.
Detailed information of all terms like Thyroid gland, Thyroxine, Triidothyronine, Calcitonine, growth and development , propylthiouracil, Calorigenesis, tadpole to frog, Oligomenorrhoea, snehal chakorkar, pharmacology, Cretinism, Myxoedema coma, Graves disease, Thiocynates, Perchlorate, Nitrates.
Radioactive iodine, I131
Introduction.
Classification .
Drugs used in Coagulant and Anticoagulant Agents
Mechanism of action .
Structure
Synthesis
Adverse Drug Reactions .
Uses.
Reference
Detailed information of all terms like Thyroid gland, Thyroxine, Triidothyronine, Calcitonine, growth and development , propylthiouracil, Calorigenesis, tadpole to frog, Oligomenorrhoea, snehal chakorkar, pharmacology, Cretinism, Myxoedema coma, Graves disease, Thiocynates, Perchlorate, Nitrates.
Radioactive iodine, I131
Introduction.
Classification .
Drugs used in Coagulant and Anticoagulant Agents
Mechanism of action .
Structure
Synthesis
Adverse Drug Reactions .
Uses.
Reference
Lipid metabolism and its disorders.pdfshinycthomas
Disorders of Lipids – Plasma lipoproteins, cholesterol, triglycerides and phospholipids in health and disease, hyperlipidemia, hyperlipoproteinemia, Gaucher’s disease, Tay-Sach’s and Niemann-Pick disease, ketone bodies.
Hypolipidaemics pharmacology with a note on Statins /Fibrates/ Sterol absorption Inhibitors/ CETP Inhibitors / Lipoprotein Lipase activators and Bile acid sequestrants
HYPERLIPIDAEMIA--LIPID PROFILE, TYPE OF HYPERLIPIDAEMIA ,LIPOPROTEINS, CLASSIFICATION OF DRUGS AND MECHANISM OF ACTION, ETIOPATHOLOGY,
METABOLISM OF LIPIDS, SIGN AND SYMPTOMS, PHARMACOKINETIC ,THERAPEUTIC USE, ADVERSE EFFECTS,CONTRAINDICATION .
Hello everyone.....I shared a pdf file containing the deep knowledge about HYPERLIPIDEMIA AND THE PHARMACOLOGY OF ANTI-HYPERLIPIDEMIC DRUGS . In the B.pharma 5th semester...there is an most important topic ANTI-HYPERLIPIDEMIC DRUGS in the subject Pharmacology -II so i uploaded this file to help the students about this most important topic.....if u want this assignment in any format....feel free to DM me on my gmail id.....careof22@gmail.com.....THANK YOU
The high risks of lipids and its relevance towards the development of different cardiovascular diseases has been known to all where this present slide focuses on that only along with the different treatment procedures,.
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These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
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ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
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- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
The hemodynamic and autonomic determinants of elevated blood pressure in obes...
Antihyperlipidemic drugs
1.
2.
“With Water, i say, 'touch me not':
to the tongue, i am tasteful;
Within limits, i am dutiful;
in excess, i am dangerous!"
The fat speaks….
3. What is Hyperlipidemia?
Hyperlipidemia a broad term, also called hyperlipo-
proteinemia, is a common disorder in developed
countries and is the major cause of coronary heart
disease.
It results from abnormalities in lipid metabolism or plasma
lipid transport or a disorder in the synthesis and
degradation of plasma lipoproteins.
4.
• Mostly hyperlipidemia is caused by lifestyle
habits or treatable medical conditions.
• Obesity, not exercising, and smoking,
diabetes, obstructive jaundice, and an under
active thyroid gland inherit hyperlipidemia.
Causes of
hyperlipidemia
5.
The biochemistry of
Plasma lipids
What are lipids?
Lipids are the heterogenous mixtures of fatty acids and
alcohol that are present in the body. The major lipids in
the bloodstream are cholesterol and it’s esters,
triglycerides and phospholipids.
6. Is C27 steroid that serves as an important
component of all cell membranes and
important precursor molecule for the
biosynthesis of bile acids, steroid hormones,
and several fat-soluble vitamins
Cholesterol
7.
What are the normal functions
of cholesterol in the body?
It is necessary for new cells to form and for older
cells to repair themselves after injury.
Cholesterol is also used by the adrenal glands to
form hormones such as cortisol, by the testicles to
form testosterone, and by the ovaries to form
estrogen and progesterone.
8.
9.
What are the normal functions of
triglycerides and Phospholipids in the
body?
• Triglycerides supply energy for the body. Triglycerides
either meet immediate energy needs in muscles or
stored as fat for future energy requirements.
• Phospholipids are compounds that are used to make
cell membranes, generate second messengers, and
store fatty acids for the use in generation of
prostaglandins
10.
What are lipoproteins?
Since blood and other body fluids are watery, so fats
need a special transport system to travel around the body.
They are carried from one place to another mixing with
protein particles, called lipoproteins.
There are four (or five) types of lipoproteins, each
having very distinct job.
11.
12.
What are lipoproteins?
A lipoprotein contains both proteins and lipids, bound to
another proteins which is called apolipoproteins, which
allow fats to move through the
water inside and outside cells.
** provide structural support
and stability, binds to receptors
Lipoprotein structure (chylomicron)
13.
14.
Classification of lipoproteins
Classification Composition Primary function
Chylomicrons Triglyceride TGs 99%,
1% protein
Transport dietary TGs to adipose
tissue & muscle
VLDL newly synthesized TGs
Lipid 90%, 10% protein
Transport endogenous TGs to adipose
tissue & muscle
IDL intermediate between
VLDL and LDL
They are not usually detectable in the
blood.
LDL Lipid 80%, 20% protein Transport endogenous cholesterol
from liver to tissues
HDL Lipid 60%, 40% protein Collect cholesterol from the body's
tissues, and take it back to the liver
19.
Hyperlipidemias are classified according to the
Fredrickson classification which is based on the
pattern of lipoproteins on electrophoresis or
ultracentrifugation. It was later adopted by the
World Health Organization (WHO). It does not
directly account for HDL, and it does not
distinguish among the different genes that may
be partially responsible for some of these
conditions.
20.
Primary or familial hyperlipoproteinaemia
Secondary hyperlipoproteinaemia
The current classification of hyperlipidemias is based
on the pattern of lipid abnormality in the blood.
GROUPS OF
HYPERLIPIDEMIA:
21.
Primary familial
hyperlipoproteinaemia
• Subclassified into six phenotypes
I , IIa , IIb, III, IV, and V based on lipoproteins and lipids
were elevated.
•current literature, however, favour the more descriptive
classifications and subclassification
see table 30.2 in foy’s book
22. Hyperlipopro
teinemia
Synonyms Increased
lipoprotein
Treatment
Type I (rare) ''Buerger-Gruetz syndrome'',
''Primary hyperlipoproteinaemia'',
or ''Familial
hyperchylomicronemia''
Chylomicro
ns by
reduced LPL
Diet control
Type IIa ''Polygenic hypercholesterolaemia''
or ''Familial hypercholesterolemia
LDL+TG Bile acid
sequestrants,
statins,
niacin
Type IIb ''Combined hyperlipidemia'' LDL and
VLDL
Statins,
niacin,
fibrate
Type III (rare) ''Familial dysbetalipoproteinemia'' IDL Fibrates,
statins
Type IV ''Familial hyperlipidemia'' VLDL Fibrate,
niacin],
statins
Type V (rare) ''Endogenous
hypertriglyceridemia
VLDL and
Chylomicro
ns
Niacin,
fibrate
23.
24. Several different classes of drugs are used toSeveral different classes of drugs are used to
treat hyperlipidemia. These classes differ nottreat hyperlipidemia. These classes differ not
only in theironly in their mechanism of actionmechanism of action but also inbut also in
the type of lipid reduction and the magnitudethe type of lipid reduction and the magnitude ofof
the reduction.the reduction.
27. Target: HMG-CoA Reductase
(HMGR)
The enzyme that
catalyzes the conversion
of HMG-CoA to
mevanolate.
This reaction is the rate-
determining step in the
synthetic pathway of
cholesterol.
+ HSCoA
H2C
C
CH3
HO
CH2
C
−
O O
C SCoA
O
H2C
C
CH3
HO
CH2
C
−
O O
H2
C OH
2NADP+
2NADPH
HMG-CoA
mevalonate
HMG-CoA
Reductase
3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA)
29.
Lovastatin was isolated from Aspergillus terreus.
Statins
Today, there are two classes of statins:
Natural Statins: Lovastatin(mevacor), Pravastatin (pravachol),
Simvastatin (Zocor).
Synthetic Statins: Atorvastatin (Lipitor), Fluvastatin (Lescol).
Statins are competitive inhibitors of HMG-CoA reductase. They
are bulky and “stuck” in the active site.
This prevents the enzyme from binding with its substrate, HMG-
CoA.
32. DRUG ADR USES
Lovastatin Increased creatinine phosphokinase,
Flatulence, Nausea
Antihyperlipoproteinemi
c agent
Simvastatin Headache, nausea, flatulence,
heartburn, abdominal pain
Antihyperlipdemic agent
Pravastatin GI disturbances, headache,
insomnia, chest pain, rash
Antihyperlipoproteinemi
c agent
Atorvastatin Headache, flatulence, diarrhea Primmary
hyperlipidemia and
secondary hyper
cholesterolemia
Rosuvastatin Headache, dizziness, constipation,
nausea, vomiting
High LDL, total
cholesterol, TGs
33. The structure should contain
a. lactone ring (sensitive to stereochemistry of it, ability of ring
to hydrolyzed, length of bridge)
b. Bicyclic rings ( could be replaced with other lipophlic rings,
size and shape of it are important for activity)
c. Ethylene bridge between them
SAR of HMG-CoA
reductase inhibitors
36. •Fibrates are antihyperlipidemic agents, widely used in the
treatment of different forms of hyperlipidemia and
hypercholesterolemia
•Fibrates are 2-phenoxy-2-methyl propanoic acid derivatives.
•these drugs stimulate β-oxidation of fatty acids in mitochondria
•This group of drugs is therefore known for decreasing plasma
levels of fatty acid and triacylglycerol
Overview
37. • Decrease plasma TGs levels more than C levels
• Fibrates lower blood triglyceride levels by reducing the
liver's production of VLDL (the triglyceride-carrying
particle that circulates in the blood) by activation of
lipoprotein lipase and speeding up the removal of TGs
from the blood. It is supported by PPAR-α.
• Fibrates also are modestly effective in increasing blood
HDL cholesterol; however, fibrates are not much
effective in lowering LDL cholesterol.
Mechanism of Action = works in a variety
ways
38.
They are classified as analogues of isobutyric acid
derivatives (essential for activity)
SAR of Fibric acid
derivatives
Fibric acid
[aromatic ring]-O-[spacer group]-C(CH3)2-CO-OH
39.
• Fenofibrate contain ester (prodrug)
• Para-subtitution with Cl or Cl containing isopropyl ring
increase half-lives.
• n-propyl spacer result in active drugs (gemfibrozil )
SAR
Fenofibrate gemfibrozil
40. DRUG ADR USES
Clofibrate Cholecystitis, gall stone,
eosinophilia, pneumonia
Type III
Hyperlipoproteinemias
Gemfibrozil Myositis syndrome,
Cholelithiasis, GI disturbances,
rash and headache.
Hyperlipidemia
Fenofibrate Headache, dizziness, asthaenia,
fatigue, arrhythmia
More potent
hypercholesterolemic
and triglycerides
lowering agent
41.
42.
cholestyramine (Questran)
colestipol hydrochloride (Colestid)
colesevelam (tablet form)
Also called bile acid–binding resins and
ion-exchange resins
Bile Acid Sequestrants
43.
• is a non-absorbed bile acid sequestrant that is
used as a therapy of hyperlipidemia and for
the pruritis of chronic liver disease and biliary
obstruction.
• is a large, highly positively charged anion
exchange resin that binds to negatively
charged anions such as bile acids.
• The binding of bile acids to cholestyramine
creates an insoluble compound that cannot be
reabsorbed and is thus excreted in the feces.
Cholestyramine (Questran)
44.
• Moderately effective with excellent safety record
• Large MW polymers containing Cl-
• Resin binds to bile acids and the acid-resin
complex is excreted
– prevents enterohepatic cycling of bile acids
– obligates the liver to synthesize replacement bile
acids from cholesterol.
• The levels of LDL-C in the serum are reduced as
more cholesterol is delivered to the liver
• Little effect on levels of HDL-C and TG.
• Excellent choice for people that cannot tolerate
other types of drugs
45.
46.
47.
A third generation drug of this class……resemble the
previous ones but don’t contain chloride ions.
Strictly speaking, it is not an anion exchange resin.
Selectivity for hydroxylated form of bile acids shows
a reduced side effect………reduced constipation.
Colesevalam
48. • Constipation
• Heartburn, nausea, bloating
• These adverse effects tend to disappear over
time.
Adverse effects
49. • Type IIa hyperlipoproteinemia.
• Relief of pruritus associated with partial biliary
obstruction (cholestyramine).
Therapeutic Uses
52. • lowers plasma cholesterol levels by inhibiting the
absorption from intestine
• This cause a decrease in the cholesterol delivery to the
liver which in turn clears more cholesterol from the
blood
• selective in its action (( not interfere with TGs, lipid-
soluble vitamins absorption))
• The levels of LDL-C in the serum are reduced as in bile
acid sequestrants.
Mechanism of action
Cholesterol Absorption
Inhibitor
53.
• as monotherapy or in combination with HMGRI for
reduction of elevated total cholesterol.
Therapeutic uses
54.
55.
NICOTINIC ACID
(Niacin)
N
COOH
NICOTINIC ACID (NIACIN)
A water soluble vitamin of the B family;
Once converted to the amide, it is
incorporated into NAD
In order to be effective, it has to be dosed at the rate of 1.5 to 3.5
gm daily.
A sustained release dosage form is available
56. Vitamin B3
Lipid-lowering properties require much higher doses than
when used as a vitamin
Effective, inexpensive, often used in combination with
other lipid-lowering drugs
Niacin (Nicotinic Acid)
57. Mechanism of action
Increases activity of lipase, which breaks down lipids
Reduces the metabolism of cholesterol and triglycerides
Indications
Effective in lowering triglyceride, total serum cholesterol,
and LDL levels
Increases HDL levels
Effective in the treatment of types IIa, IIb, III, IV, and V
hyperlipidemias
Niacin (Nicotinic Acid)
58.
Adverse effects
Flushing (due to histamine release)
Pruritus
GI distress
Liver dysfunction and jaundice. Serious liver
damage is the most important risk.
Niacin (Nicotinic Acid)
59.
• Molecule has two tertiary butylphenol groups linked
by a dithiopropylidene bridge, giving it a high
lipophilic character with strong antioxidant
properties.
LDL oxidation inhibitor
probucol
61.
In humans, it causes reduction of both liver and serum
cholesterol levels, but it does not alter plasma triglycerides.
It reduces LDL
It reduces to a lesser extent HDL levels by a unique
mechanism that is still not clearly delineated.
The reduction of HDL may be caused by the ability of
probucol to inhibit the synthesis of apoprotein A-1, a major
protein component of HDL.
It is effective at reducing levels of LDL and is used in
hyperlipoproteinemias characterized by elevated LDL
levels.
ADR: GI disorders and prolongation of GI intervals.
Use: It is used as antihyperlipoproteinemic agent.
62.
Sitosterol is a plant sterol, whose structure is identical with
that of cholesterol, except for the substituted ethyl group on
C-24 of its side chain.
Miscellaneous agent
β-Sitosterol
63.
Although the mechanism of its hypolipidemic effect is not
clearly understood, it is suspected that the drug inhibits the
absorption of dietary cholesterol from the gastrointestinal
tract.
Sitosterols are absorbed poorly from the mucosal lining and
appear to compete with cholesterol for absorption sites in
the intestine.
ADR: Diarrhoea, constipation, GI disturbances
Use: Anti cholesteremic agent and treatment of prostatic
oedema.
Editor's Notes
75% phospholipids
20%cholesterol
5%glycolipids
Type I hyperlipidemia is quite uncommon
It is also called familial hyperchylomicronemia and Buerger-Gruetz syndrome.
is due to deficiency of lipoprotein lipase (LPL) or
altered apo lipoprotein C2, resulting in elevated chylomicrons, the particles that transfer fatty acids from the digestive tract to the liver. Its occurrence is 0.1% of the
population.
the most common form, is further classified into type IIa and type IIb, depending mainly on whether there is elevation in the triglyceride level in addition to LDL cholesterol.
Type IIa
Familial hypercholesterolemia
This may be sporadic (due to dietary factors), polygenic, or truly familial as a result of a mutation either in the LDL receptor gene on chromosome 19 (0.2% of the population) or the ApoB gene (0.2%).
Type IIb
Familial combined hyperlipoproteinemia (FCH)
The high VLDL levels (due to overproduction of substrates, including triglycerides). And also high LDL (caused by the decreased clearance of LDL).
III
is due to high chylomicrons and IDL (intermediate
density lipoprotein).
It is also known as broad beta disease or dysbetalipoproteinemia,.
It is due to cholesterol-rich VLDL.
IV
also known as hypertriglyceridemia or pure
hypertriglyceridemia, is due to high triglycerides.
V
is very similar to type I, but have high VLDL in
addition to chylomicrons. This disease has glucose intolerance and hyperuricemia.