BIO 212 – Exam 3
Bio 212 Course Notes – Exam 3
Ch 30-34 – Cardiovascular Disorders—6/11 & on
Ch 36-37 – Respiratory Disorders—6/25 & 6/27
*Exam open 6/28-7/2*
• Arteries, away.
• Venules veins.
o Thinner walls, lumen = bigger.
Ch 30 – Disorders of Blood Flow in the Systemic Circuit
***Review Ch 29 and pgs 739-741 if needed
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
1
, BIO 212 – Exam 3
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
2
, BIO 212 – Exam 3
smoking
o 2nd - Drugs to lower lipoproteins
• Almost always many lifestyle choices… especially Americans! Woohoo!
o First treatment should be change ur life!
3
, BIO 212 – Exam 3
▪ 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—keep comin back!
• 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
4
Bio 212 Course Notes – Exam 3
Ch 30-34 – Cardiovascular Disorders—6/11 & on
Ch 36-37 – Respiratory Disorders—6/25 & 6/27
*Exam open 6/28-7/2*
• Arteries, away.
• Venules veins.
o Thinner walls, lumen = bigger.
Ch 30 – Disorders of Blood Flow in the Systemic Circuit
***Review Ch 29 and pgs 739-741 if needed
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
1
, BIO 212 – Exam 3
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
2
, BIO 212 – Exam 3
smoking
o 2nd - Drugs to lower lipoproteins
• Almost always many lifestyle choices… especially Americans! Woohoo!
o First treatment should be change ur life!
3
, BIO 212 – Exam 3
▪ 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—keep comin back!
• 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
4
