Biochemistry Flashcards
1) Which amino acid is the precursor for NO synthesis?
Nitric oxide is synthesized in the conversion of L-arginine to L-citrulline in a reaction catalzyed by nitric oxide synthase.
2) Which is the greatest component of surfactant at term?
a) phosphatidyl choline
b) phosphatidylglycerol
c) phosphatidylinositol
A Phosphatidylcholine. Phosphatidylcholine composes 70% of surfactant. The remainder of surfactant is 8% neutral lipids (cholesterol), 8% phosphatidylglycerol, 8% other phospholipids, 8% protein.
3) Which enzyme does the fetus have that the placenta doesn’t
a) 17 hydroxylase
b) 3bhydroxylase
c) sulfatase
A – 17-hydroxylase is not present in placenta; as a consequence the placenta must synthesize estrogens from DHEAS supplied by the fetal adrenal glands.
4) Precursor for fetal steroid synthesis
4) The placenta efficiently transports LDL so that the fetus can use maternally derived cholesterol for steroid synthesis. Cholesterol is not the rate-limiting step in steroidogenesis in the fetus.
5) What is the substrate for oxidative metabolism of the placenta:
a) ketone bodies
b) lactate
c) fatty acids
d) glucose
Glucose- principal substrate for oxidate metabolism in the placenta
6) Which cytokine is anti-inflammatory?
a) IL-10
b) IL-8
c) IL-6
d) IL-1
e) TNF-alpha
6) A. IL-10. IL-10 & TGF-B are anti-inflammatory cytokines.
7) What is the precursor for the increased estriol concentrations seen immediately preceding term birth?
a) fetal adrenal cortisol
b) fetal adrenal DHEA-S
c) maternal progesterone
B. Fetal adrenal DHEAS. Fetal adrenal DHEAS supplies the substrate for the placenta produce estrogens as the placenta lacks the 17-alpha-hydroxylase enzyme to produce estrogens from cholesterol. Fetuses that lack adrenal glands (such as in anencephaly) have markedly reduced estrogne levels.
8) What is the precursor of fetal adrenal steroids?
a) LDL
b) Amino acids
c) Glutathione
d) Vitamin D
LDL
9) What is 11-deoxycorticosterone a precursor of?
a) Aldosterone
b) DHEAS
B. Fetal adrenal DHEAS. Fetal adrenal DHEAS supplies the substrate for the placenta produce estrogens as the placenta lacks the 17-alpha-hydroxylase enzyme to produce estrogens from cholesterol. Fetuses that lack adrenal glands (such as in anencephaly) have markedly reduced estrogne levels.DHEAS is synthesized from cholesterol → pregnenolone → 17-OH-pregnenolone → DHEA. This requires 17-alpha hydroxylase (missing from placenta), sulfatase.
10) The by-product of carbohydrate metabolism is NOT
a) CO2
b) H2O
c) NH3
d) Lactic acid
D In glycolysis, one glucose molecule is broken down into pyruvate + 2 H+ + 2 water molecules + 2 ATP. Aerobic metabolism will result in CO2, anaerobic will result in lactate.
NH3 is a byproduct of protein metabolism.
10) The by-product of carbohydrate metabolism is NOT
a) CO2
b) H2O
c) NH3
d) Lactic acid
D In glycolysis, one glucose molecule is broken down into pyruvate + 2 H+ + 2 water molecules + 2 ATP. Aerobic metabolism will result in CO2, anaerobic will result in lactate.
NH3 is a byproduct of protein metabolism.
11) Where is the main source for PGE2 and PGF2 in pregnancy?
The decidua mainly produces PGF2alpha and PGE2. The myometrium synthesizes prostacycline. The amnion synthesize PGE2.
12) Cyclic AMP and uterine contractions
12) Increases in cAMP concentrations cause a de-activation of myosin light chain kinase. Deactivating myosin light chain kinase prevents myosin-actin ATPase activity and prevents uterine contractions. Therefore increased cAMP concentrations cause uterine relaxation.
13) Mechanism for uterine contractions
Uterotonins bind to G-protein coupled cell surface receptor, which
-activates phospholipase C to convert phospatidylinositol triphosphate to inositol triphosphate
- which release calcium from the sarcoplasmic reticulum. - - - Calcium then binds to calmodulin
- the calcium-calmodulin complex then activates myosin light chain kinase.
- - - Myosin light chain kinase phosphorylates myosin light chain, which enables the ATPase activity & causes sliding of myosin over actin fibrils.
15) Mechanism of action of beta mimetics, oxytocin
Beta-mimetics (terbutaline) bind to a G-protein coupled receptor and increase cAMP. Oxytoxin (and other uterotonins) bind to a G-protein coupled receptor that activates phospholipase C.
