BIO 212 – Exam 3 Study Guide
Ch 30-34 – Cardiovascular Disorders
Ch 36-37 – Respiratory Disorders
Arteries, away.
Venules veins.
Thinner walls, lumen = bigger.
Ch 30 – Disorders of Blood Flow in the Systemic Circuit
Review Ch 29
Disorders of Arterial Circulation
Diseases of the arterial system cause impaired blood flow. The effect of the impaired
blood flow depends on the structures involved and extent of the altered flow.
Ischemia – reduction in arterial flow to a level that does not meet the oxygen
demands for a tissue
Infarction – an area of ischemic necrosis in an organ
Hyperlipidemia
A state of elevated lipids in the blood that is associated with increased
risk of atherosclerosis and its associated risks of heart attack and stroke
o Elevated lipids… hyperlipidemia.
Decrease lipids to get better.
Apoproteins throughout this structure
Lipoproteins
o Core of triglycerides and cholesterol surrounded by phospholipids and
apoproteins which dictate the interactions and metabolic fate of the lipoprotein
o 4 types
Chylomicrons – 80-90% triglycerides, 2% protein
Largest, synthesized in the small intestine
Transport dietary triglycerides and cholesterol that are
absorbed through the GI tract
Triglycerides are transferred to adipose and skeletal muscle cells
Cholesterol is taken up by the liver which synthesizes into VLDL or
secretes it with bile
VLDL – very low density lipoproteins
55-65% triglycerides, 10% cholesterol, 5-10% protein
, Synthesized in the liver
Transport endogenous triglycerides produced by the liver to
adipose and skeletal muscle cells
Then form IDL which are transported back to the liver and
recycled into VLDL or converted to LDL
Primary energy source during fasting
LDL – low density lipoproteins
10% triglycerides, 50% cholesterol , 25%
protein Synthesized in the blood
Main cholesterol carrier, “bad
cholesterol” Two pathways of removal
o Receptor dependent
o Scavenger
HDL – high density lipoproteins
5% triglycerides, 20% cholesterol, 50%
protein Synthesized in the liver
“Good cholesterol”
Transport cholesterol from the tissues back to the liver
Etiologies: multifactorial, genetics, nutrition, lifestyle, other diseases, medications o
Primary hypercholesterolemia – independent of other diseases or health
problems
Strong genetic component
Ex: familial hypercholesterolemia type 2A – deficient LDL receptors
o Secondary hypercholesterolemia – associated with other disease or
lifestyle Strong lifestyle component – poor diet, lack of exercise
Other diseases: Type II diabetes mellitus, metabolic
syndrome, hypothyroidism
Diagnosis
o Fasting lipoprotein profile which measures LDL, HDL triglycerides
and total cholesterol
o Total cholesterol > 200 mg/dL or HDL < 40 mg/dL – follow up
profile Treatment
o 1st - Lifestyle changes – increased exercise, changes to diet, lose
weight, stop smoking
o 2nd - Drugs to lower lipoproteins
Almost always many lifestyle choices… especially Americans!
Woohoo! o First treatment should be change ur life!
, Triglycerides will change! Which will in turn, change cholesterol
levels, More exercise HDL increase. Good!
o Sugar is the worst! “by far the worst dietary thing we’ve done to our people and
country” Mid to late 80s, war on fat…
Atherosclerosis
The formation of fibro-fatty lesions in the intimal lining of the large and
medium sized arteries
o Cardiovascular disease is a common complication and is the leading
cause of death in males and females in the US
o Silent killer – plaques begin to form in your 20’s but do not manifest until
20-40 years later
Etiologies and risk factors
o Hypercholesterolemia
o Age
o Genetics
o Male, post menopausal females
o High serum glucose, Type 2 diabetes mellitus
o Hypertension (HTN)
o Obesity, sedentary lifestyle
o Smoking
o High stress levels
o Inflammation
Increased CRP
o Increased homocysteine
o Infections – Chlamydia pneumonia, herpesvirus, cytomegalovirus
Pathogenesis
1. Damaged endothelium
2. Inflammation and adhesion of monocytes and platelets occur
3. Monocytes migrate into the tunica intima and transform into
macrophages which begin to engulf LDL – forming foam cells
4. Oxidation of LDL occurs with increases damage and causes growth
factors to be released
5. Growth factors stimulate SMCs to multiply and invade the lining
6. Leads to the formation of a plaque – stable or unstable
Depends on cap, core size, level of inflammation
Oxidize! Release toxic/free radicals! Antioxidants for
diets! Plaque formation
Ch 30-34 – Cardiovascular Disorders
Ch 36-37 – Respiratory Disorders
Arteries, away.
Venules veins.
Thinner walls, lumen = bigger.
Ch 30 – Disorders of Blood Flow in the Systemic Circuit
Review Ch 29
Disorders of Arterial Circulation
Diseases of the arterial system cause impaired blood flow. The effect of the impaired
blood flow depends on the structures involved and extent of the altered flow.
Ischemia – reduction in arterial flow to a level that does not meet the oxygen
demands for a tissue
Infarction – an area of ischemic necrosis in an organ
Hyperlipidemia
A state of elevated lipids in the blood that is associated with increased
risk of atherosclerosis and its associated risks of heart attack and stroke
o Elevated lipids… hyperlipidemia.
Decrease lipids to get better.
Apoproteins throughout this structure
Lipoproteins
o Core of triglycerides and cholesterol surrounded by phospholipids and
apoproteins which dictate the interactions and metabolic fate of the lipoprotein
o 4 types
Chylomicrons – 80-90% triglycerides, 2% protein
Largest, synthesized in the small intestine
Transport dietary triglycerides and cholesterol that are
absorbed through the GI tract
Triglycerides are transferred to adipose and skeletal muscle cells
Cholesterol is taken up by the liver which synthesizes into VLDL or
secretes it with bile
VLDL – very low density lipoproteins
55-65% triglycerides, 10% cholesterol, 5-10% protein
, Synthesized in the liver
Transport endogenous triglycerides produced by the liver to
adipose and skeletal muscle cells
Then form IDL which are transported back to the liver and
recycled into VLDL or converted to LDL
Primary energy source during fasting
LDL – low density lipoproteins
10% triglycerides, 50% cholesterol , 25%
protein Synthesized in the blood
Main cholesterol carrier, “bad
cholesterol” Two pathways of removal
o Receptor dependent
o Scavenger
HDL – high density lipoproteins
5% triglycerides, 20% cholesterol, 50%
protein Synthesized in the liver
“Good cholesterol”
Transport cholesterol from the tissues back to the liver
Etiologies: multifactorial, genetics, nutrition, lifestyle, other diseases, medications o
Primary hypercholesterolemia – independent of other diseases or health
problems
Strong genetic component
Ex: familial hypercholesterolemia type 2A – deficient LDL receptors
o Secondary hypercholesterolemia – associated with other disease or
lifestyle Strong lifestyle component – poor diet, lack of exercise
Other diseases: Type II diabetes mellitus, metabolic
syndrome, hypothyroidism
Diagnosis
o Fasting lipoprotein profile which measures LDL, HDL triglycerides
and total cholesterol
o Total cholesterol > 200 mg/dL or HDL < 40 mg/dL – follow up
profile Treatment
o 1st - Lifestyle changes – increased exercise, changes to diet, lose
weight, stop smoking
o 2nd - Drugs to lower lipoproteins
Almost always many lifestyle choices… especially Americans!
Woohoo! o First treatment should be change ur life!
, Triglycerides will change! Which will in turn, change cholesterol
levels, More exercise HDL increase. Good!
o Sugar is the worst! “by far the worst dietary thing we’ve done to our people and
country” Mid to late 80s, war on fat…
Atherosclerosis
The formation of fibro-fatty lesions in the intimal lining of the large and
medium sized arteries
o Cardiovascular disease is a common complication and is the leading
cause of death in males and females in the US
o Silent killer – plaques begin to form in your 20’s but do not manifest until
20-40 years later
Etiologies and risk factors
o Hypercholesterolemia
o Age
o Genetics
o Male, post menopausal females
o High serum glucose, Type 2 diabetes mellitus
o Hypertension (HTN)
o Obesity, sedentary lifestyle
o Smoking
o High stress levels
o Inflammation
Increased CRP
o Increased homocysteine
o Infections – Chlamydia pneumonia, herpesvirus, cytomegalovirus
Pathogenesis
1. Damaged endothelium
2. Inflammation and adhesion of monocytes and platelets occur
3. Monocytes migrate into the tunica intima and transform into
macrophages which begin to engulf LDL – forming foam cells
4. Oxidation of LDL occurs with increases damage and causes growth
factors to be released
5. Growth factors stimulate SMCs to multiply and invade the lining
6. Leads to the formation of a plaque – stable or unstable
Depends on cap, core size, level of inflammation
Oxidize! Release toxic/free radicals! Antioxidants for
diets! Plaque formation
