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Angina (Angina Pectoris)
chest pain due to decreased O2 to the heart
Ischemia
lack of blood supply/decreased oxygenation
Necrosis
tissue death
Plaque
accumulated deposits of fats/other substances in blood vessels & start causing problems
Arteriosclerosis
narrowing & hardening of blood vessels
results from healing process and normal part of aging (scar forms from healing of damaged tissue = hardening)
Atherosclerosis
accumulation of fatty plaques inside blood vessels
as the plaques grow, cause partial/complete occlusions
Thrombosis
formation of blood clot in blood vessel
Embolism
blood clot has broken free & traveling in blood vessels of body
Myocardial Infarction
heart attack
aka MI/AMI
Heart
A hollow, four-chambered muscular organ that pumps blood throughout the body
mediastinum
The heart is located in thoracic cavity between the lungs in
Epicardium, Myocardium, Endocardium
3 layers of the heart
Epicardium
outer layer of heart
contains nerve fibers
Myocardium
middle layer of heart
heart muscle; contraction
Endocardium
inner layer of heart
blood vessels that supply blood to middle layer
upper right and left atria
lower right and left ventricles
4 chambers of the heart
left ventricle
Which ventricle is more muscular to help pump oxygenated blood out of the heart to the tissues
Coronary circulation
Right and left coronary artery
Coronary sinus
3 sources of blood
Coronary circulation
flow of blood to and from the tissues of the heart
heart receives oxygenated blood from 2 main sources, which feed directly off the aorta
Right and Left Coronary Artery
both branch into 2 arteries, which supply both ventricles, as well as the right and left atrium
provide oxygenated blood to heart
Coronary sinus
collective name given to the location where all the veins of the heart (containing deoxygenated blood) drain into
drains into the heart through an opening in the right atrium
Cardiac cycle
the events surrounding the filling and emptying of the chambers of the heart, which are coordinated by an electrical conductive system
1. Sinoatrial Node (SA node)
2. Atrioventricular node (AV node)
3. Atrioventricular bundle (bundle of HIS)
4. Purkinje fibers
Components of the Cardiac Cycle

Sinoatrial node (SA node)
pacemaker of the heart
initiates cardiac cycle, by producing an electrical pulse that spreads over both atria and causes them to simultaneously contract and force blood into the ventricles
Purkinje fibers
stimulation causes ventricles to contract simultaneously
Acute Myocardial Infarction
sudden heart attack that results from dead heart muscle tissue that is unable to contract in rhythm
occlusion of blood flow due to clot or dislodged particle(s) that prevent blood flow to tissue
Non-modifiable risk factors of CHD
family history (first degree)
gender
age
Modifiable risk factors of CHD
smoking
diet & nutrition
elevated blood pressure
obesity
exercise
lifestyle
stress
endogenous cholesterol
cholesterol manufactured in the liver
exogenous cholesterol
cholesterol obtained from diet
saturated fats and trans fats
fats that are solid at RT
raises cholesterol levels, causing atherosclerosis
unsaturated fats
fats that are liquid at RT
lower plaque-forming cholesterol
"good" mono: olive, canola, omega-3 oils
"good" poly: soybean, sunflower, corn oils
pancreatic lipase
enzyme that breaks down exogenous cholesterol in small intestine
lipoprotein lipase (LPL)
Exogenous fats are broken down further in the blood by what enzyme?
breakdown of chylomicrons → chylomicrons remnants or VLDL, then VLDL → LDL
HMG-CoA reductase
enzyme responsible for the synthesis of endogenous cholesterol (VLDL and HDL) in the liver
Lipid functions in the body
Hormone production (steroid hormones (fat-based))
Structural (cells have phospholipid cellular membrane)
Vitamin Transport
Insulation (maintain body temp)
Skin maintenance (protect/maintain health skin)
Organ and nerve production (myelin sheath made of lipids; provides cushion for organs to prevent damage)
Energy source (can use lipids for energy)
Satiation (feeling of fullness in body)
insoluble; solube
Lipids are __________ in plasma and _________ in organic solvents
Chylomicrons, VLDL, LDL, HDL
4 types of lipoproteins
protein, cholesterol esters, cholesterol, triglycerides, phospholipids
components that make up each type of lipoproteins
Fatty Acid-Binding Protein (FABP)
Soluble protein that binds to lipids that are broken down in the intestine so they can be transported through the blood as micelle-like structures to the liver
Chylomicrons
lipoprotein synthesized in the small intestines
after synthesis, delivered to muscle / fat tissue or returns to liver for excretion or recycling
largest lipoprotein
highest fat (triglycerides) content
lowest density/protein
triglycerides
Chylomicrons predominately combine with which fat?
VLDL, LDL, HDL
Which lipoprotein(s) are made in the liver?
Very Low Density Lipoprotein
What does VLDL stand for?
VLDL
lipoprotein synthesized in the liver
"very lousy" lipoprotein
comes from chylomicrons
second highest percent of triglycerides
Low Density Lipoprotein
What does LDL stand for?
LDL
lipoprotein synthesized in the liver
"lousy" lipoprotein
comes from breakdown of VLDL by LPL
highest percent of cholesterol & cholesterol esters
High Density Lipoprotein
What does HDL stand for?
HDL
lipoprotein synthesized in the liver
"GOOD" lipoprotein that removes plaque from tissues/arteries helping to decrease the risk of atherosclerosis
highest density/protein
Chylomicrons
lipoprotein responsible for thick and creamy appearance (lipemia) in serum of NON-FASTING pts
VLDL
lipoprotein responsible for thick and creamy appearance in serum of FASTING pts
LDL
lipoprotein that contributes to development of atherosclerosis
HDL
lipoprotein associated with a decrease risk of atherosclerosis
Lechin:Cholesterol Acyltransferase (LCAT)
enzyme responsible for the process of converting soluble lipoprotein molecules to less soluble molecules (turns into ester)
joins fatty acid to chylomicron, VLDL, or LDL molecules and esterifies them → less soluble → HDL binds → moves to liver (excreted / recycled)
Apoproteins
protein portion of lipoproteins that provide transport of lipids in the body
made in the liver
HDL and VLDL
apoproteins are made in the liver and are packed with which lipoproteins as they are released from the liver
Apolipoprotein A-I
apoprotein found on 90% HDL that activates LCAT
chromosome 11
Apoprotein A-I is found on what chromosome?
B-100
apolipoprotein found on LDL and VLDL
chromosome 2
B-48 and B-100 is found on what chromosome?
B-48
apolipoprotein found on chylomicrons
when chylomicron gets degraded in circulation it will stay attached which allows the liver to recognize and take care of it
Apoprotein C-1
activates LCAT and is located on chylomicrons, VLDL, and HDL
Apoprotein C-2
important cofactor for LPL and is located on chylomicrons, VLDL, and HDL
Apoprotein C-3
inhibitor of LPL
responsible for hydrolysis of triglycerides in chylomicrons to form remnants of chylomicrons or VLDL, and then LDL
Apoprotein E
aids in the uptake of chylomicron remnants in the liver and is located on chylomicrons, VLDL, and HDL
Primary/Familial and Secondary
2 types of Hyperlipoproteinemia
Primary/Familial Hyperlipoproteinemia
elevated lipids where no underlying disease is present
can be inherited
1. in-born errors of metabolism
2. increased levels of LDL and HDL
2 causes of Primary Hyperlipoproteinemia
Familial Hypercholesterolemia
Hypertriglyceridemia
Familial Hypertriglyceridemia
3 types of Primary Hyperlipoproteinemia
Familial Hypercholesterolemia
Metabolic disorder caused by problem with B-100 receptor molecule on the LDL molecule that results in body's inability to breakdown LDL molecules allowing them to accumulate
Results in increase in serum levels of LDL
1. decrease/complete absence of LDL receptors
2. inability of receptors to bind with LDL
3. inability of receptor to internalize LDL into cell
3 causes of Familial Hypercholesterolemia
Hypertriglyceridemia
excessive amount of triglycerides in the blood due to deficiency in LPL
increased levels of chylomicrons cause lipemic serum even in fasting state when LPL absent
elevated serum levels of triglycerides = 500 mg/dL
Familial Hypertriglyceridemia (FHTG)
amount of VLDL molecules is normal, but the size of the particle is enlarged
usually an increase in total cholesterol, but LDL levels are usually normal
fairly common disorder
Secondary Hyperlipoproteinemia
elevated lipids caused by an underlying disorder
results when excess lipids are not removed/used, and then deposit and accumulate in tissue and arterial walls, preventing blood flow to vital organs
Causes of Secondary Hyperlipoproteinemia
Diabetes mellitus
Medications
Nephrotic syndrome and Chronic renal failure
Hepatic disorders including biliary obstruction
Acute and Stress related conditions
Hypothyroidism
hyperlipidemia
present in ALL hyperproteinemia
clear
Interpretations of Serum Appearance
Triglycerides normal or near normal (
hazy to turbind
Interpretations of Serum Appearance
Triglycerides moderately elevated (approx. 300-500 mg/dL)
opaque to milky
Interpretations of Serum Appearance
Triglycerides exceeding 600 mg/dL
pre-menopausal women
people who exercise regularly
people who maintain a low but healthy weight
High HDL-cholesterol levels are associated with (3):
high LDL and low HDL
LDL and HDL levels in:
post menopause (low estrogen)
hypothyroidism (low thyroxine)
diabetes, type II (low insulin)
Hypoalphalipoproteinemia
the absence or a non-detectable level of Apolipoprotein A-I, leading to a decreased/absent levels of HDL
low HDL = no removal of bad lipids
Tangier's disease
Disease associated with absence or deficiency of A-I apoprotein
LCAT is unable to function and esterification of cholesterol is diminished → leads to increase LDL in circulation with no HDL action to remove
Atherosclerosis, MI, and strokes
resulting medical conditions of Tangier's disease
Coronary Heart Disease (CHD)
plaque build-up and blockage of blood vessels from excessive LDL
Apolipoprotein isoenzyme E4
apolipoprotein isoenzyme associated with Alzheimer's disease
Apolipoprotein isoenzyme E2
apolipoprotein isoenzyme that is a marker for increased atherosclerosis and possible stroke and MI
Abetalipoproteinemia
rare, genetic disorder with an absence of lipoproteins containing apolipoprotein B
diagnosed in infancy with fat absorption problems and difficulty gaining weight and growth (failure to thrive)
chylomicrons, VLDL, or LDL
Abetalipoproteinemia leads to no detectable levels of which lipoproteins?
acanthocytes
Hematological findings in abetalipoproteinemia include RBC membrane defects, including
severe vision, neurological and mobility problems
Without treatment, abetalipoproteinemia will lead to development of: