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WorksheetsCardio Exam 2 - Pathophys
Total questions: 49
Worksheet time: 25mins
Name
Class
Date
1.
What are some functions of lipids
a)
energy
b)
growth
c)
protection
d)
insulation and skin protection
e)
absorption of lipids
2.
Which type of lipid is the precursor for androgens, estrogens, progesterone, adrenocorticoids and bile acids
a)
cholesterol
b)
cholesterol fatty acid ester
c)
triglyceride
d)
phospholipid
3.
Which type of lipid is cholesterol ester hydrolase break ester bond to form cholesterol
a)
cholesterol
b)
cholesterol fatty acid ester
c)
triglyceride
d)
phospholipid
4.
Which type of lipid is a highly concentrated stores of metabolic energy and are hydrolyzed by lipase enzymes when required for energy production
a)
cholesterol
b)
cholesterol fatty acid ester
c)
triglyceride
d)
phospholipid
5.
Which type of lipid make up amphipathic compounds that are used to make cell membranes, generate secondary messengers, and store fatty acids for use in the generation of prostaglandins
a)
cholesterol
b)
cholesterol fatty acid ester
c)
triglyceride
d)
phospholipid
6.
What are the 2 major roles of fatty acids
a)
stored as triglycerides
b)
component of membrane phospholipids
c)
cellular energy
7.
What is the main source of free fatty acids
a)
blood
b)
sunlight
c)
diet
d)
storage
8.
Most free fatty acids are non-essential except
a)
linoleic acid
b)
linolenic acid
c)
arachidic acid
d)
stearic acid
e)
palmitic acid
9.
What disease comes from Vitamin A deficiency
a)
xerosis
b)
blindness
c)
Ricket's disease
d)
osteomalacia
e)
hypocalcemia
10.
What disease comes from Vitamin D deficiency
a)
xerosis
b)
blindness
c)
Ricket's disease
d)
osteomalacia
e)
hypocalcemia
11.
What disease comes from Vitamin E deficiency
a)
xerosis
b)
blindness
c)
increased fragility of erythrocytes
d)
peripheral neuropathy
e)
bleeding disorders
12.
What disease comes from Vitamin K deficiency
a)
xerosis
b)
blindness
c)
increased fragility of erythrocytes
d)
peripheral neuropathy
e)
bleeding disorders
13.
Pancreatic lipase breaks down
a)
triglycerides to diglycerides
b)
diglycerides to monoglycerides
c)
monoglycerides to free fatty acids
d)
triglycerides to chylomicrons<br />
14.
Where does triglycerides get broken down to diglycerides
a)
intestine
b)
exogenous
c)
enterocyte
d)
endogenous
15.
Where do monoglycerides get broken down into free fatty acids
a)
intestine
b)
exogenous
c)
enterocyte
d)
endogenous
16.
What does the drug Alli (orlistat) inhibit in order to treat obesity
a)
pancreatic lipase
b)
NPC1L1 receptor blocker
c)
ACAT
17.
What does the drug Ezetimibe inhibit
a)
pancreatic lipase
b)
NPC1L1 receptor blocker
c)
ACAT
18.
What does Acyl CoA drugs inhibit
a)
pancreatic lipase
b)
NPC1L1 receptor blocker
c)
ACAT
19.
What are some characteristics of bile salts
a)
synthesized in the liver
b)
stored in the gallbladder and released into the small intestine
c)
help absorb some cholesterol, fatty acids and fat soluble vitamins
d)
regulates their own synthesis and conversion of cholesterol
20.
Bile salts helps in the emulsification of fat and absorption of fat droplets
a)
true
b)
false
21.
The polar side of the bile salt helps <br />
a)
with the interaction with aqueous compartment
b)
with Van der Waals interaction with lipids
22.
The nonpolar side of the bile salt helps<br />
a)
with the interaction with aqueous compartment
b)
with Van der Waals interaction with lipids
23.
What do micsosomal triglyceride transfer protein (MTTP) react with to form chylomicrons
a)
triglycerides
b)
cholesterol ester
c)
phospholipids
d)
apoproteins
24.
Lipoproteins are
a)
macromolecules containing lipid substances bound with protein
b)
amphipathic molecules that solubilizes lipids
c)
chylomicrons
d)
VLDL, IDL, LDL
e)
HDL
25.
Which lipoprotein carries triglycerides from the intestine to the liver, skeletal muscle and adipose tissue
a)
chylomicrons
b)
VLDL
c)
IDL
d)
LDL
e)
HDL
26.
Which lipoprotein carries newly synthesize triglycerides from liver to adipose tissue
a)
chylomicrons
b)
VLDL
c)
IDL
d)
LDL
e)
HDL
27.
Which lipoprotein is the intermediate between VLDL and LDL that is not usually detectable in the blood
a)
chylomicrons
b)
VLDL
c)
IDL
d)
LDL
e)
HDL
28.
Which lipoprotein carries cholesterol from the liver to cells of the body (aka bad cholesterol, major circulating form of cholesterol)
a)
chylomicrons
b)
VLDL
c)
IDL
d)
LDL
e)
HDL
29.
Which lipoprotein collects cholesterol from the body's tissues and bring it back to liver for degradation (aka good cholesterol)
a)
chylomicrons
b)
VLDL
c)
IDL
d)
LDL
e)
HDL
30.
Which lipoprotein has the highest protein composition
a)
chylomicrons
b)
VLDL
c)
IDL
d)
LDL
e)
HDL
31.
Which lipoprotein has the highest cholesterol composition
a)
chylomicrons
b)
VLDL
c)
IDL
d)
LDL
e)
HDL
32.
Which lipoprotein has the highest triglycerides composition
a)
chylomicrons
b)
VLDL
c)
IDL
d)
LDL
e)
HDL
33.
What are some roles of apoproteins
a)
transport of lipoproteins
b)
activation of enzymes
c)
receptor binding
d)
regulates their own synthesis and conversion of cholesterol
34.
Which apoprotein is on chylomicrons
a)
E
b)
C2
c)
B48
d)
B100
e)
A-1
35.
Which apoprotein is on chylomicrons remnant
a)
E
b)
C2
c)
B48
d)
B100
e)
A-1
36.
Which apoprotein is on VLDL
a)
E
b)
C2
c)
B48
d)
B100
e)
A-1
37.
Which apoprotein is on IDL
a)
E
b)
C2
c)
B48
d)
B100
e)
A-1
38.
Which apoprotein is on LDL
a)
E
b)
C2
c)
B48
d)
B100
e)
A-1
39.
Which apoprotein is on HDL
a)
E
b)
C2
c)
B48
d)
B100
e)
A-1
40.
What are some characteristics of Apo B48
a)
exogenous
b)
export chylomicrons from intestine
c)
endogenous
d)
ligand for LDL receptor
41.
What are some characteristics of Apo B100
a)
exogenous
b)
export chylomicrons from intestine
c)
endogenous
d)
ligand for LDL receptor
42.
What is familial hypercholesterolemia caused by
a)
Apo B100 mutation
b)
LDL-R is defective
c)
PSCK9 is overactive
43.
A common life-threatening genetic condition, Apo B100 mutation, makes the body unable to remove ___ from circulation
a)
chylomicrons
b)
VLDL
c)
IDL
d)
LDL
e)
HDL
44.
What drugs can inhibit PCSK9 enzymes to combat familial hypercholesterolemia
a)
Alirocumab
b)
Evolocumab
c)
Zetia
45.
What are the roles of Apo E
a)
receptor ligand
b)
clears remnants
c)
IDL
d)
dysbetalipoproteinmia
46.
A mutation in Apo E leads to
a)
Apo B100 mutation
b)
activation of enzymes
c)
hypercholesterolemia
d)
dysbetalipoproteinmia
47.
What is the role of Apo C
a)
receptor ligand
b)
clears remnants
c)
IDL
d)
dysbetalipoproteinmia
e)
lipoprotein lipase
48.
What causes hypertriglyceridemia
a)
mutation in LPL
b)
Apo C2 deficiency
c)
hypercholesterolemia
d)
dysbetalipoproteinmia
49.
What enzymes do ApoA1 activate
a)
pancreatic lipase
b)
NPC1L1 receptor blocker
c)
ACAT
d)
LCAT
e)
CERP
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