Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Unit 7 > MCP non-structure questions > Flashcards

MCP non-structure questions Flashcards

1
Q

breakdown of glycogen to glucose

A

glycogenolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

glucose polymer humans cannot digest

A

cellulose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

organ responsible for maintaining blood glucose levels

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

sugar polymer containing 2-15 sugars

A

olgiosacch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

disaccharidase that cleaves glucose dimers with alpha 1-4 linkage

A

maltase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

type of enzyme that cleaves sugar polymers at internal linkages

A

endoglycosidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

non glucose component of lactose

A

galactose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

oxidation of glucose to produce ATP

A

glycolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

first enzyme to act in carb digestion

A

amylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

table sugar= glucose + ____

A

fructose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

branched polysacch in starch

A

amylopectin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

humans store glucose as the polymer ___

A

glycogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

disaccharidase that cleaves table sugar

A

sucrase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

type of enzyme that cleaves sugar-sugar linkages

A

glycosidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

brush border enzyme that cleaves alpha dextrins to glucose and isomaltose

A

glucoamylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

source of digestive enzymes in mouth

A

salivary gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

glucose disacch with alpha 1,6 glycosidic bond

A

isomaltose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

branched oligosacch products of amylopectin digestion

A

dextrins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

hormone signaling that blood glucose is low

A

glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

hormone signaling that blood glucose is high

A

insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

organ that synthesizes digestive enzymes for the small intestine

A

pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

(hexokinase/glucokinase) has a very high affinity for glucose

A

hexokinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the purpose behind glucokinase’s low affinity for glucose

A

it only converts when glucose levels are very high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

when the cell needs energy, ___ enters glycolysis

A

G6P

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

which enzyme plays a central role in regulation of glycolysis

A

PFK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

the rxn catalyzed by PGK is an example of what type of reaction

A

substrate level phosphorylation (also the PK reaction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

net gain of glycolysis

A

2 ATP
2 NADH
2 pyruvate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

fructose in the muscle is converted to F6P by (hexokinase/glucokinase)

A

hexokinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

fructose in the liver is converted to GAP by (hexokinase/glucokinase)

A

glucokinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

deficiencies in F1P aldolase cause (2 things)

A

liver damage and hypoglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

a deficiency in galactokinase results in galactitol formation which causes

A

cataracts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

a deficiency in UMP transferase causes (two things)

A

mental retardation, liver failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

simple treatment for UMP transferase deficiency

A

screen newborns, then eliminate lactose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

cost of temporarily storing glu units in glycogen in the muscle: G6P > glycogen > G6P

A

1 ATP to prime G1P for glycogen synthase
.1 ATP to convert 10% of units released from 1-6 linkages as glu to G6P
total: 1.1 ATP per G6P

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

cost of temporarily storing glu units in glycogen in the liver: Glu > glycogen > Glu

A

1 ATP to convert glu to G6P
1 ATP to prime G1P for glycogen synthase
total: 2 ATP per glu

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

(Von Gierke/Anderson) dz: defective glucose-6-phosphatase or transport system, affects liver and kidney

A

Von Gierke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

(Von Gierke/Anderson) dz: defective branching enzyme (alpha 1,4 > alpha 1,6), affects liver and spleen

A

Anderson

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

in Von Gierke dz, glycogen is (increased/decreased), with a normal structure

A

increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

clinical features of Von Gierke dz

A

massive enlargement of liver, failure to thrive, severe hypoglycemia, ketosis, hyperuricemia, hyperlipemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

clinical features of Anderson dz

A

progressive cirrhosis of liver, liver failure causes death, usually before age 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

McArdle dz has a defective ____ enzyme and affects muscles

A

phosphorylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

clinical features of McArdle dz

A

limited ability to perform strenuous exercise because of painful muscle cramps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

glycogen is (increased/decreased) in McArdle dz, with normal structure

A

moderately increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

why is glycogen synthesis and breakdown tightly regulated

A

to avoid a futile cycle (cost!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what type of enzyme catalyzes cleavage of fructose 1,6 bisphosphate into DHAP and GAP

A

aldolase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

(glycogen synthesis/glycolysis): phosphoglucomutase plays a direct role

A

glycogen synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

enzyme that catalyzes conversion of G6P to F6P

A

isomerase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

which enzyme has a phosphotidyl intermediate: (enolase/ lactate dehydrogenase/phosphoglycerate mutase)

A

phosphoglycerate mutase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

amino acid precursor of dopamine

A

tyrosine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

amino acid precursor of epi

A

tyrosine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

amino acid precursor of GABA

A

glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

amino acid precursor of histamine

A

histidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

amino acid precursor of melanin

A

tyrosine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

amino acid precursor of melatonin

A

tryptophan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

amino acid precursor of norepi

A

tyrosine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

amino acid precursor of serotonin

A

tryptophan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

amino acid precursor of niacin

A

tryptophan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

amino acid precursor of thyroxine

A

tyrosine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

rate limiting step in catecholamine biosynthesis

A

tyrosine hydroxylation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

clinical correlation: Parkinson’s patients are treated with ____ since it will cross the BBB and hopefully increase production of ____

A

DOPA, dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

dopamine formation requires which cofactor: (pyridoxal phosphate/Vitamin C)

A

pyridoxal phosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

norepi formation requires which cofactor: (pyridoxal phosphate/Vitamin C)

A

Vitamin C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

catechols are degraded by an enzyme called:

A

monoamide oxidase (MAO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

clinical correlation: inhibitors of monoamide oxidase (MAO) are used as _______

A

anti depressants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

clinical correlation: defect in biosynthesis of melanins causes:

A

albinism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

clinical correlation: deficiency in tryptophan that leads to a niacin def

A

Pellagra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

four D’s of Pellegra

A

dermatitis, dementia, diarrhea, death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

the body needs ____ for: formation of methionine from homocysteine, biosynthesis of purines and pyrimidines, biosynthesis of glycine

A

one carbon groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

biotin is a carrier of ___

A

CO2, the most oxidized one carbon group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

THF is a carrier of ___

A

one carbon groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

sulfa drugs inhibit the synthesis of ____ by bacteria

A

folate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

what is the purpose of the poly-gamma-glutamyl side chain on folic acid?

A

keeps folic acid trapped inside cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

formation of N5-methyl form of THF is (reversible/irreversible) in humans

A

irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

clinical correlation: patients who are deficient in the enzyme that makes the N5 form of THF have a higher risk of ___ and a lower risk of ____

A

higher risk of atherosclerosis/heart disease

lower risk of colon cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

folate deficiency affects what type of tissues, and what is the first symptom

A

rapidly dividing tissues/cells, first symptom is anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

three drugs that give you folate def

A

oral contraceptives, barbiturates, methotrexate (chemo)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

clinical correlation: birth defect from folate def

A

spina bifida

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

clinical correlation: elevated levels of homocysteine are strongly correlated with increased risk of:

A

atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

clinical correlation: def of cystathionine synthase, children die by age three or four of heart disease or stroke

A

homocystinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

clinical correlation: def of cystathionase

A

cystathioninuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

clinical correlation: def of THF and B12 leads to:

A

megablastic anemia, immature RBCs are released into circulation, pernicious

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

__ def is associated with demyelination and degeneration of the spinal cord, usually seen when there is a problem with intrinsic factor

A

B12 (intrinsic factor carries B12 from gut into blood stream)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

clinical correlation: B12 def causes folate def, but then folate is supplemented. Result is neurological problems but no anemia

A

Folate trap

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

enzyme that cleaves FBP into DHAP and GAP

A

aldolase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

phosphoglucomutase plays a direct role in (glycolysis/glycogen synthesis)

A

glycogen synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

enzyme that converts G6P to F6P

A

isomerase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

enzyme with a phosphohistidyl intermediate (enolase/glycogen synthase/phosphoglycerate mutase)

A

phosphoglycerate mutase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

three organs where mitochondria are most plentiful

A

heart, kidney, liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

clinical correlation: Vit B1 def (pyruvate builds up), TPP is needed for reaction

A

Beri Beri

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

clinical correlation: dihydrolipoamide is the site of action of ____ poisoning

A

arsenite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

the succinyl CoA > succinate reaction illustrates the ____ principle

A

common intermediate principle (product of first reaction is substrate for second reaction, couples an exergonic rxn to an endergonic rxn)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

why is it good that the oxidation of malate by NAD+ is difficult so very little OAA is in in eqbm with a lot of malate?

A

so malate can exit to cytoplasm during resting state and serve as a substrate for gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

a membrane transport system is present in the IMM to transport (NADH/CO2/pyruvate)

A

pyruvate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

the reaction catalyzed by aconitase in TCA cycle is: (condensation-hydrolysis/dehydration-rehydration)

A

dehydration-rehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

which enzyme illustrates common intermediate principle (hexokinase/adenylate kinase/succinyl CoA synthetase)

A

succinyl CoA synthetase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

during respiration, you need lots of (NAD/NADP)

A

NAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

for detox and biosynthesis, you need lots of (NAD/NADP)

A

NADP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

clinical correlation: two consequences of G6PDH def

A

favism (hemolytic anemia), advantage where malaria is endemic (most common enzyme def)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

pyruvate carboxylase is found where specifically

A

only in mitochondria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

the only aa’s that cannot contribute to gluconeogenesis (two)

A

Leu and Lys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

acetyl CoA from ____ and ___ cannot contribute to gluconeogenesis

A

fatty acids and aa’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

biotin is bound to which enzyme (PEPCK/G6phosphatase/pyruvate carboxylase)

A

pyruvate carboxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

which enzyme does not function in reversible nonoxidative phase of pentose phosphate shunt (epimerase/isomerase/lactonase/transaldolase/transketolase)

A

lactonase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

which kinase in glycolysis functions reversibly in gluconeogenesis

A

phosphoglycerate kinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

if O2 is not available for mitochondrial respiration, the ETC will:

A

stop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

if O2 supply is blocked then suddenly restored, cyt c would begin shifting toward its oxidized state (before/after) the pool of coenzyme Q would shift toward its oxidized state

A

before

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

(cyt c/NAD+/ubiquinone/FeS): acts as a mobile H+/e- carrier in a Mitchell Loop type of direct coupling mechanism between e- transfer and H+ transport across a membrane layer

A

ubiquinone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

(ubiquinone/cyt c) is the e- donating substrate for cytochrome oxidase

A

cyt c

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

(cyt c/FeS/FMN/CuB) can accept 2 e- per turnover

A

FMN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

the three catalytic subunits of F1 are (independent/cooperative)

A

cooperative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

(ADP/Pi/O2/CO2) enters the mit matrix through an electroneutral transporter driven by the change in pH component of the electrochem gradient

A

Pi (O2 and CO2 diffuse, ADP is exchanged with ATP by electrical potential, not H potential)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

(pyruvate DHase/pyruvate kinase/phosphorylase kinase/glycogen synthase) is inactivated when blood sugar increases and insulin is released

A

phosphorylase kinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

F26BP activates (FBPase/PFK)

A

PFK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

following phosphorylation by protein kinase A, phosphorylase kinase activates (glycogen branching enzyme/glycogen phosphorylase/glycogen synthase/phosphoprotein phosphatase)

A

glycogen phosphorylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

three benefits to storing energy as fat

A

1-lower oxidation state than carbons in carbs or protein
2-stored without bound water
3-don’t participate in cell’s osmotic balance so cells can store enormous amounts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

myristic fatty acid has _ carbons and _ dbs

A

14 carbons, no dbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

palmitic fatty acid has _ carbons and _ dbs

A

16, no dbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

palmitoleic fatty acid has _ carbons and _ dbs

A

16, 1 db

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

stearic fatty acid has _ carbons and _ dbs

A

18, 0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

oleic fatty acid has _ carbons and _ dbs

A

18, 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

linoleic fatty acid has _ carbons and _ dbs

A

18, 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

linolenic fatty acid has _ carbons and _ dbs

A

18, 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

arachidonic fatty acid has _ carbons and _ dbs

A

20, 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

clinical correlation: failure of bile production or blockage of bile flow, exocrine pancreas dysfunction or obstruction of pancreatic duct, failure of uptake into intestinal mucosal cells cause:

A

fatty stool

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

fatty acids are released from lipoproteins by the action of ______ (enzyme) located in the capillary endothelial walls of muscle and adipose tissue

A

lipoprotein lipase

126
Q

hepatic lipase processes ___

A

LDL

127
Q

oxidation of triacylglycerols to CO2 and H2O yields 9kcal/g while carbohydrate yields __kcal/g

A

4

128
Q

pancreatic lipase catalyzes the partial hydrolysis of ____

A

triglycerides

129
Q

entry of nonesterified long chain fatty acids from the intestinal lumen into the intestinal mucosa is mediated by:

A

protein carriers

130
Q

major constituents of ____ are cholesterol, bile salts, and phosphatidylcholine

A

bile

131
Q

excess lipid in feces is called

A

steatorrhea

132
Q

a def in lipoprotein lipase would most likely cause abnormalities in (digestion of fat in intestine/unloading of free fatty acids from VLDL/synthesis of VLDL/synthesis of chylomicrons)

A

unloading of free fatty acids from VLDL

133
Q

Apo__ in mature chylomicrons is recognized by lipoprotein lipase

A

ApoCII

134
Q

albumin has bound (triglycerides/non esterified fatty acids)

A

non esterified fatty acids

135
Q

(triglycerides/non esterified fatty acids) are found in substantial amounts free in solution

A

neither

136
Q

lipoproteins contain lots of (triglycerides/non esterified fatty acids)

A

triglycerides

137
Q

mixed micelles contain (non esterified fatty acids/triglycerides/both)

A

non esterified fatty acids

138
Q

mnemonic for ten essential amino acids

A

PVT. TIM HALL

139
Q

ten essential amino acids

A

Phe, Val, Thr, Trp, Ile, Met, His, Arg, Leu, Lys

140
Q

cystein becomes essential if ____ (aa) is low

A

methionine

141
Q

tyrosine becomes essential if ____ (aa) is low

A

Phe

142
Q

clinical correlation: patients defective in pancreatic enzymes, must supplement with pancreatic enzymes

A

CF

143
Q

clinical correlation: a defect in the transport system for neutral and aromatic aa’s including Trp from the gut and renal tubules. Niacin def, diarrhea, dermatitis, dementia, death, find neutral and aromatic aa’s in urine and feces

A

Hartnup’s disease

144
Q

clinical correlation: def in transport system for basic aa’s and cystine from gut and renal tubules, UTI’s and kidney stones, treat with fluids and penicillamine

A

cystinuria

145
Q

urinary levels of which compound can provide a measure of muscle protein breakdown

A

3-methyl histidine

146
Q

(children and convalescing adults/diseases of wasting and starvation) show positive nitrogen balance

A

children (growing) and convalescing adults (rebuilding)

147
Q

(children and convalescing adults/diseases of wasting and starvation) show negative nitrogen balance

A

diseases of wasting and starvation

148
Q

names with “glut” usually have _ carbons (#)

A

5

149
Q

amino acid degradation is located in the (mitochondria/cytoplasm) for urea cycle

A

mit

150
Q

amino acid degradation is located in the (mitochondria/cytoplasm) for pyrimidine nucleotide biosynthesis

A

cytoplasm

151
Q

pyridoxal phosphate is vitamin B_

A

B6

152
Q

essential cofactor for all transaminations

A

pyridoxal phosphate B6

153
Q

__ (aa) can be easily made from pyruvate, efficient way to send 3 carbon groups back to liver to be easily converted into glucose while disposing of an NH4+ grp, one of most abundant aa’s in blood

A

Ala

154
Q

__ (aa) is one of most abundant aa’s inside cells, transaminases converge on it, and through oxidative deamination you can make energy from ripping off the NH4+

A

glutamate

155
Q

glutamate is mainly deaminated in the (muscles/liver/blood)

A

liver

156
Q

most common defect in urea cycle

A

OTC defect (X linked gene)

157
Q

four benefits of using urea to dispose

A

1-carries two ammonia groups
2-soluble
3-non protonable–keeps solution pH 7.2
4-low reactivity

158
Q

how is the urea cycle regulated

A

nitrogen balance

159
Q

protein free diet: levels of urea cycle enzymes (increase several fold/decrease)

A

decrease

160
Q

high protein diet: levels of urea cycle enzymes (increase several fold/decrease)

A

increase several fold

161
Q

clinical correlation: sign of OTC defect

A

ammonia intoxication

162
Q

if citrulline builds up in the urea cycle, what happens to the individual

A

mental retardation

163
Q

arginine is an essential amino acid for what process in children

A

growth

164
Q

in the urea cycle, (alpha keto glutarate/aspartate/carbomyl phosphate) is generated from CO2 and NH4+

A

carbomyl phosphate

165
Q

clinical correlation: Pellagra’s disease can be the result of ____ disease

A

Hartnup’s disease (def of niacin)

166
Q

the two most abundant aa’s inside our cells

A

glutamate and glutamine

167
Q

transamination of alanine by alanine transaminase generates (fumarate/acetyl CoA/pyruvate)

A

pyruvate

168
Q

which aa? easily converted to Pro, synthesized from ornithine in urea cycle, glucogenic aa that can be converted to alpha ketoglutarate

A

arginine–also, essential for growth

169
Q

glutamate is the precursor for which NT

A

GABA

170
Q

clinical correlation: irritability, vomiting, lethargy, confusion, resp distress, migraines are all symptoms of _____ toxicity

A

ammonia toxicity

171
Q

(ketogenic/glucogenic): aa’s are degraded to either acetyl CoA or acetoacetyl CoA

A

ketogenic–give rise to ketone bodies

172
Q

(ketogenic/glucogenic): aa’s are degraded to pyruvate or TCA cycle intermediates

A

glucogenic–give rise to glucose via formation of phosphoenolpyruvate

173
Q

brain’s preferred energy source

A

glucose

174
Q

acetyl CoA can be converted to (fatty acids/glucose/both)

A

fatty acids

175
Q

cofactor in conversion of glycine to serine

A

THF

176
Q

enzyme used to degrade branched chain amino acids

A

BCAT: branched chain aa transaminase

177
Q

clinical correlation: ____ (enzyme) def in mice shows increased insulin sensitivity, increased protein turnover, increased serum Leu levels, decreased fat and body weight, increased energy expenditure

A

BCAT–Leucine builds up

178
Q

clinical correlation: defect in branched chain keto acid DHase, build up of keto acids give urine a characteristic odor, tx by restricting keto amino acids (Val, Leu, Ile) or administering high doses of thiamine

A

maple syrup urine disease/branched chain ketoaciduria

179
Q

clinical correlation: a genetic disorder assoc with inability to catalyze hydroxylation of Phe and build up of toxic derivatives of Phe (phenylpyruvate), mental retardation in infants if not detected early

A

PKU–phenylketonuria

180
Q

tx for PKU

A

restrict Phe in diet until at least 16 years old

181
Q

maternal PKU

A

mother has PKU and isn’t being treated, in utero levels are high

182
Q

clinical correlation: defect in homogentisate oxidase, deposits in cartilage causes arthritis at a young age, diagnose by looking through earlobe at darkened cartilage

A

alkaptonuria

183
Q

clinical correlation: high levels of homocysteine, high risk of atherosclerosis, oxidizes LDL

A

homocystinuria

184
Q

treatment for homocystinuria

A

PLP cofactor

185
Q

(proline/arginine) is synthesized and degraded through the same pathway

A

proline

186
Q

serine (is glucogenic/can be made from aspartate)

A

is glucogenic

187
Q

maple syrup urine disease caused by defect in (alpha keto acid DHase/phenylalanine hydroxylase)

A

alpha keto acid DHase

188
Q

PKU caused by defect in (alpha keto acid DHase/phenylalanine hydroxylase)

A

Phe hydroxylase

189
Q

Ala, Ser, Cys, Gly, Thr can all be degraded into:

A

pyruvate

190
Q

vitamin B12 is found in the (hydroxy/adenosyl) form in methylmalonic acid mutase

A

adenosyl

191
Q

when THF builds up as N5 methyl THF

A

folate trap

192
Q

what donates the methyl group in conversion of NE to epi

A

SAM (S adenosylmethionine)

193
Q

three amino acids that require B12 for the degradation of their carbon skeletons

A

Val, Ile, Met

194
Q

spinal cord degeneration and other neuro problems during B12 def (can be cured by administration of folic acid/are caused by a deficiency in the conversion of methylmalonyl CoA to succinyl CoA)

A

are caused by a deficiency in the conversion of methylmalonyl CoA to succinyl CoA

195
Q

most reduced form of THF (N5 methyl/N5 formyl)

A

N5 methyl

196
Q

not made from tyrosine (dopamine/melanin/serotonin/NE)

A

serotonin

197
Q

HMG-CoA reductase is (more active in fed state than fasted state/less active in fed state than fasted state)

A

more active in fed state

198
Q

glycogen phosphorylase is (more active in fed state than fasted state/less active in fed state than fasted state)

A

less active in fed state

199
Q

pyruvate kinase is (more active in fed state than fasted state/less active in fed state than fasted state)

A

more active in fed state

200
Q

acetyl CoA carboxylase is (more active in fed state than fasted state/less active in fed state than fasted state)

A

more active in fed state

201
Q

liver PFK-2 is (more active in fed state than fasted state/less active in fed state than fasted state)

A

more active in fed state

202
Q

hormone sensitive lipase is is (more active in fed state than fasted state/less active in fed state than fasted state)

A

less active in fed state

203
Q

in going from an overnight fast to prolonged starvation, glycolysis in the brain (increases/decreases)

A

decreases

204
Q

in the basal state, which contributes over half the kcal used (glucose/fatty acids)

A

fatty acids

205
Q

coritsol promotes but epi inhibits (gluconeo in liver/glycogen synthesis in liver)

A

glycogen synthesis

206
Q

when epi is released due to excitement, (dephosphorylation of perilipin in adipocytes/liver degrades glycogen and makes glucose)

A

liver degrades glycogen and makes glucose via gluconeogenesis

207
Q

(high/low) energy and glucose levels are associated with decreased activity of cAMP dependent protein kinase

A

low

208
Q

enzymes required during (fed/fasting) states are activated by phosphorylation

A

fasting

209
Q

basal state: (feeding/fasting)

A

fasting

210
Q

synthesis of triacylglycerols in adipocytes: (fasting/feeding)

A

feeding

211
Q

elevated insulin/glucagon ratio: (fasting/feeding)

A

feeding

212
Q

highest rate of fatty acid uptake by liver cells: (fasting/diabetes type I)

A

diabetes type I

213
Q

lowest rate of muscle proteolysis: (feeding/starvation)

A

feeding

214
Q

maximal production of acetoacetate by liver (starvation/diabetes type I)

A

diabetes type I

215
Q

intermediate of major significance in nucleotide metabolsim

A

PRPP (an activated ribose ready for base attachment)

216
Q

(azaserine/sulfonamide) blocks amide transfer from glutamine

A

azaserine (an analog of glutamine), inhibits IMP synthesis

217
Q

(azaserine/sulfonamide) blocks biosynthesis of folic acid in bacteria and prevents its formation, blocking nucleotide synthesis

A

sulfonamide

218
Q

IMP converted to (AMP/GMP) requires seven phosphoanhydride bonds

A

AMP

219
Q

IMP converted to (AMP/GMP) requires eight phosphoanhydride bonds

A

GMP

220
Q

what is the rate determining step of IMP synthesis

A

first two steps, feedback inhibition

221
Q

clinical correlation: patients with ____ (enzyme) def build up high levels of pyrimidines in their serum and urine, first step is rate limiting step and excess carbamoyl phosphate that builds up is converted to pyrimidines

A

OTC def (urea cycle)

222
Q

ribonucleotide reductase is present in (all cells all the time/replicating cells during replication)

A

replicating cells during replication

223
Q

clinical correlation: ribonucleotide reductase is inhibited by ____, a potent chemotherapy agent

A

hydroxyurea

224
Q

(F-UMP/methotrexate) looks like a uracil but a fluorine at the 5 position causes permanent (suicide) inhibition

A

F-UMP/5-Fluorouracil

225
Q

(F-UMP/methotrexate) is an analog of folic acid that blocks regeneration of THF

A

methotrexate

226
Q

molybdenum is required in trace amounts in humans because ______ (enzyme in purine degradation) uses it

A

xanthine oxidase

227
Q

clinical correlation: def of adenosine deaminase in purine degradation leads to what condition that can be treated with gene therapy

A

SCID–severe combined immunodef

228
Q

xanthine oxidase generates _____

A

superoxide

229
Q

clinical correlation: the enzymes required to degrade pyrimidines also are used to clear which chemo agent

A

5-Fluorouracil–if you are def in this enzyme (no clinical signs) and get cancer and use 5-F as your chemo, you will die from the treatment

230
Q

clinical correlation: due to overactive PRPP or partially deficient HGPRT (X linked)

A

gout

231
Q

clinical correlation: caused by precipitation of sodium urate crystals in joints and kidneys

A

gout

232
Q

clinical correlation: treat ___ with allopurinol which blocks the production of uric acid

A

gout

233
Q

allopurinol inhibits which enzyme used in the production of uric acid

A

xanthine oxidase

234
Q

clinical correlation: ____ (drug) is often given as a pretreatment for chemo to prevent uricemia

A

allopurinol

235
Q

clinical correlation: complete lack of HGPRT activity, X linked recessive, severe

A

Lesch-Nyhan syndrome

236
Q

clinical correlation: symptoms include hyperuricemia, gout, urinary tract stones, MR, spasticity, self mutilation

A

Lesch-Nyhan syndrome

237
Q

clinical correlation: treatment of _____ with allopurinol reduces the uric acid formation but does not alleviate the neurological symptoms

A

Lesch-Nyhan syndrome

238
Q

clinical correlation: adenosine deaminase def

A

severe combined immuno def SCID

239
Q

clinical correlation: treat this by bone marrow transplant and enzyme replacement, gene therapy is experimental

A

SCID

240
Q

clinical correlation: genetic disorder of pyrimidine synthesis, ___ acid accumulates in blood and is excreted in urine, alleviated by feeding of uridine or cytidine

A

orotic aciduria

241
Q

(methotrexate/5-Fluorouracil) leads to the inhibition of thymidylate synthase

A

5-Fluorouracil

242
Q

(sulfonamide/azaserine) blocks the synthesis of GMP from IMP, blocks synthesis of CTP from UTP

A

azaserine

243
Q

HGPRT is used to salvage (pyrimidine/purine) nucleotides

A

purine

244
Q

allopurinol is often given to patients in conjunction with chemo because (it inhibits salvage of purines/the destruction of cancer cells releases large amounts of purines)

A

the destruction of cancer cells releases large amounts of purines

245
Q

the (purine/pyrimidine) ring is formed directly on the ribose phosphate

A

purine

246
Q

because glutamine is used in multiple steps during purine synthesis, this pathway is inhibited by (azaserine/sulfonamides)

A

azaserine

247
Q

GTP is made using (N5 methyl THF/phosphoribosyl pyrophosphate)

A

phosphoribosyl pyrophosphate

248
Q

pyrimidines are made from (carbamoyl phosphate and aspartate/ribonucleotide reductase and thymidylate synthase)

A

carbamoyl phosphate and aspartate

249
Q

sulfonamides (inhibit PRPP synthase/are analogs of p-amino benzoic acid)

A

are analogs of p-amino benzoic acid

250
Q

5-Fluorouracil leads to inhibition of (dihydrofolate reductase/thymidylate synthase)

A

thymidylate synthase

251
Q

de novo synthesis of AMP requires (GTP and ATP/5-methyl THF)

A

GTP and ATP

252
Q

thymidylate synthase (requires dihydrofolate reductase for maximal activity/converts dUTP to dTTP)

A

requires dihydrofolate reductase for maximal activity

253
Q

(glucagon/insulin) signals the cell to take up fat and store it

A

insulin

254
Q

role of perilipins

A

form a shield around TG to block enzymatic action

255
Q

how are perilipins removed

A

when the they are phosphorylated by cAMP dependent PKA, they are removed

256
Q

how is hormone sensitive lipase activated

A

by phosphorylation by cAMP dependent PKA (same as perilipin–convenient!)

257
Q

what does insulin do to hormone sensitive lipase

A

it deactivates it by dephosphorylating it by upregulating a phosphatase

258
Q

cAMP is activated by (insulin/glucagon/epi/NE)

A

glucagon, epi, NE

259
Q

when free fatty acids are released inside the adipocyte, how do they get to the blood

A

attach to adipocyte lipid binding protein, travel through blood attached to albumin

260
Q

what type of receptor is the glucagon receptor on the fat cell

A

GPCR (goes to adenlyl cyclase, to cAMP, to PKA, to enzymes)

261
Q

(delta/omega) nomenclature: start counting at end (not the acid end)

A

omega

262
Q

(delta/omega) nomenclature: start counting at beginning (the acid end)

A

delta

263
Q

the second db in omega nomenclature is usually _ carbons later

A

3

264
Q

(palmitoleic and oleic/linoleic and linolenic) fatty acids are essential (we can’t make them de novo)

A

linoleic and linolenic

265
Q

CPT1 in carnitine shuttle is inhibited by

A

malonyl CoA (intermediate in FA synthesis)

266
Q

enzyme in fatty acid activation in first part of beta ox

A

acyl-CoA synthetase/thiokinase

267
Q

three steps in the beta ox of fatty acids are catalyzed by:

A

one multifunctional protein with all three enzymes

268
Q

clinical correlation: def in medium chain acyl CoA dehydrogenase, see symptoms in (hyper/hypo) glycemia

A

hypoglycemia (because that’s when you need to really start breaking down fatty acids)

269
Q

symptoms of medium chain acyl CoA DHase def:

A

liver dysfunction, seizures, coma

270
Q

(6/8) ATP oxidized per carbon in glycolysis

A

6

271
Q

(6/8) ATP oxidized per carbon in beta ox

A

8

272
Q

where are KB’s made specifically (organ and organelle) and where are they used?

A

made in liver mitochondria

used NOT in liver

273
Q

KB’s are made during starving or when there’s no glucose in diet because the TCA cycle is (active/stalled)

A

stalled–so what to do with the acetyl CoA’s building up? Make KB’s!

274
Q

KB (over/under) production occurs in Type I diabetes

A

over production

275
Q

clinical correlation: when KB’s build up in blood

A

ketoacidosis, blood gets acidic, coma (Type I diabetes)

276
Q

why does ketoacidosis not occur in Type II diabetes

A

there is some insulin still

277
Q

ATP yield from complete beta ox of palmitic acid

A

129 ATP

278
Q

ATP yield from complete beta ox of palmitoleic acid (16:1 delta 9)

A

127 ATP

279
Q

where would you find adipocyte lipid binding protein

A

in adipose tissue and many other tissues

280
Q

where would you find HMG-CoA lyase

A

liver tissue (NOT adipose)

281
Q

where would you find glycerol kinase

A

liver and sometimes adipose tissue

282
Q

carbons in TGs have a (higher/lower) oxidation state than carbons in carbs or proteins, so the are worth more energy

A

lower

283
Q

TG’s are stored (bound to water/unbound)

A

unbound

284
Q

TG’s (do/don’t) participate in the cell’s osmotic balance

A

do not–so you can store lots

285
Q

after a fatty meal, what happens to your serum

A

milky serum

286
Q

medium chain fatty acids are found in what body secretion

A

breast milk

287
Q

NEFA

A

non esterified fatty acids aka free fatty acids

288
Q

brain (can/cannot) use free fatty acids as fuel

A

cannot–BBB prevents transport

289
Q

four fat soluble vitamins

A

DAKE

290
Q

role of bile in fat digestion

A

emulsifies the fat droplet so enzymes can access the bonds

291
Q

activation of pancreatic lipase requires formation of a complex with:

A

colipase and a droplet of emulsified lipid

292
Q

a pancreatic lipase cleaves the TG into

A

two free fatty acids and one monoacyl glycerol (the middle one stays on)

293
Q

stool in CF

A

fatty because pancreatic lipase can’t get out of the pancreas to digest fats

294
Q

important Apoprotein for chylomicron formation

A

B48

295
Q

tag on chylomicron for lipoprotein lipase

A

CII

296
Q

enzyme that clears chylomicrons from the capillaries

A

lipoprotein lipase

297
Q

products of lipoprotein lipase

A

3 non esterified fatty acids and 1 glycerol

298
Q

(lipoprotein lipase/pancreatic lipase) digests the TG into two free fatty acids and one MAG

A

pancreatic lipase

299
Q

chylomicrons are (slowly/rapidly) cleared from the serum

A

rapidly

300
Q

VLDLs have a (shorter/longer) circulating half life than chylomicrons. They are also broken down by lipoprotein lipase

A

longer

301
Q

clinical correlation: severe calorie def, no subcutaneous fat, gross loss of muscle, easily wrinkled skin, thin dry hair, apathy/anxiety

A

marasmus

302
Q

treatment for marasmus

A

avoid refeeding syndrome–give small meals at frequent intervals

303
Q

clinical correlation: edematous malnutrition, severely def in protein

A

Kwashiorkor

304
Q

(marasmus/Kwashiorkor): pale skin with burn like lesions, cyanotic extremities, brittle hair, hepatomegaly, irritability, edema, hypoglycemia

A

Kwashiorkor

305
Q

conversion of acetyl CoA to ketone bodies yields slightly (more/less) energy than oxidation in TCA cycle

A

slightly less energy

306
Q

BMI less than 18.5 is classified by WHO as

A

underweight

307
Q

BMI 18.5-24.9 is classified by popular description as

A

healthy, normal

308
Q

BMI 25-29.9 is classified by WHO as

A

grade 1 overweight (overweight)

309
Q

BMI 30-39.9 is classified by WHO as

A

grade 2 overweight (obese)

310
Q

BMI 40+ is classified by WHO as

A

grade 3 overweight (morbidly obese)

Unit 7 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions