Previous exam topics Flashcards

1
Q

what is an acid?

A

proton donator
(its dissociation makes conj base)

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

what is a base?

A

proton acceptor
(its dissociation makes a conj acid)

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

weak acids and bases exist in:

A

equilibrium with conj species

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

what is an example of a weak acid and base?

A

acid: carboxylic acid
base: amine

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

what is the most imp physiological buffer

A

bicarbonate

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

what bonds are in 2,3,4 protein structure?

A

hydrogen bonds and non covalent bonds

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

when do buffers work best?

A

at pKa

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

what is secondary amino acid structure?

A

a- helix and b-sheets

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

what holds primary protein structure together?

A

covalent bonds

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

what is an oncones?

A

mutation at one amino acid

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

what happens in M phase

A

mitosis

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

amino acids determine?

A

protein folding

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

what occurs during G1

A

interphase, increases in size, and is active biochemically
(technically G1, S and G2 are interphase)

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

what are key features of 2nd messagner systems?

A

specificity
amplification
augmentation
rapid signal transduction

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

the goblins have what structure?

A

no beta structure, a helix connected by turns

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

what occurs with sickle cell disease?

A

gu becomes val
makes hydrophobic

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

most cells are in the ______ stage of cell cycle

A

G0

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

what happens during s phase?

A

cell copies DNA makes sister chromatids

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

What is an oncogene

A

Mutation that takes place at a single amino acid
Example RAS G12V mutation

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

What happens at the G1 phase?

A

Longest, cell grows and makes new proteins and organelles

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

what happens during G2 phase

A

cell prepares for mitosis by growing and syn new proteins and lipids

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

What Happens during the S phase?

A

Synthesis phase, DNA replicates making Sister cromatids

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

What occurs at the m phase

A

Mitosis

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

What are some things that occur during apoptosis?

A

•Outer Membrane blebbing
•Shrinking
•Condensation of the nucleus
•Fragmentation of chromosomes
•Formation of cytoplasmic vacuoles
•The cell fragments generated by apoptosis are taken up and
eliminated by neighboring cells and phagocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
give a brief summary of extrinsic apoptotic signaling
mediated by cell death receptors formation of disc recruitment of pro-casp 8 activation of effector caspases 3,6,7 can feed into intrinsic from here
26
give a brief summary of intrinsic apoptotic signaling
-marked by central event: MOMP -release of cytochrome C -trigger of complex of caspase 9 and APAF1 via CARD and APAF1 -Casp 9 recruits effector caspases 3,6,7
27
what will happen with loss of function in CASP8 mutations?
suppress apoptotic signaling allowing cell survival
28
what is rRNA syn by?
syn by RNA polymerase I
29
what does rRNA do?
rRNA + protein= ribosomes transferred to cytoplasm to become parts of large and small sub units of ribosome
30
what is tRNA syn by?
RNA poly III
31
what does tRNA do?
-carry amino acids to ribosomes, -anticodon sequence is complementary to mRNA being read
32
when is a tRNA said to be charged?
when the correct amino acid is attached to the 3' end
33
what is mRNA?
made from DNA used as template for protein syn
34
what is the TCA cycle?
uses acetyl coA to make ATP and water
35
coenzyme A needs which vitamin?
pantothenic acid
36
what steps of TCA need coA?
1,4,5
37
what kind of pathway is TCA?
amphibolic, meaning it does catabolism and anabolism
38
what are the main points of entrt of electrons from fuel ox to enter ETC?
Compex 1 and 2 (e- collect at coQ)
39
what ratios change the ETC?
high NADH/NAD slows high ATP/ADP slows
40
what are some inhibitors of TCA?
barbiturates 1, antimycin A- 3, cyanide 4, oligomycin atp synthase blocker
41
how is fat mobilization regulated?
adenylate cyclase helps it enter, triacylglycerol lipase hydrolyzes bonds to release FA and glycerol
42
what tissues do not really use FA and which ones use a lot?
nervous not a lot muscle a lot
43
what helps transfer FA from adipose to other tissues?
albumin
44
what is needed to transport FA into mitochondria?
carnitine palmitoyl transferases (CPT1)
45
what prevents CPT1?
malonyl CoA (makes sense cause if FA syn is happening you dont want them to be broken down right away)
46
what is the most important type of fatty acid oxidation?
B- ox
47
what is the important enzyme of b-ox?
acytyl co-a dehydrogenase
48
what inhibits acyl coA dehydrogenase?
hypogycin (from unripe fruit of ackee tree)
49
where do you get most ATP?
b ox of palmitate
50
where does ketone body formation occur?
mitocondria
51
what is the major site of acetoacetate formation and why?
liver because it is where HMG CoA synthase
52
during fasting what two things are increased?
fat mobilization and ketogenesis (ketone body formation)
53
how are dietary lipids digested early?
lingual lipase in mouth gastric lipase in stomach
54
what are the essential FA?
lineoic l-lineoic archidonic
55
how are FA digested in small intestine?
*pancreatic lipase co-lipase bicarbonate bile salt
56
bile sat is most useful in what form?
anionic form
57
what is the function of co-lipase?
attract and anchor pancreatic lipase to surface of emulsion particle
58
once in the small intestine what happens to the FA?
carried by bile salt, make mixed micelle, cross epithithealial boarder, and the FA and 2-MG reforms TGs, can make chylomicrons
59
what can occur if there is a lipid malabsorption?
steatorrhea
60
ldl has the most:
cholesterol and chol esters
61
Chylomicrons and vldl has the most:
TGs
62
what does A-I do
activator of LCAT, choI pick up
63
what does B-100 do?
LIGANT FOR LDL receptor
64
what does C-II do?
activates LPL
65
what does apoprotein E do?
Ligand for LDL and chylomicron remnant
66
what does LPL do?
processing chymicrons
67
what is difference between Lcat and Acat?
Lcat in bLood with HDL
68
what is difference between HSL and LPL?
H is fat mobiLization L is fat storage
69
what happens to chylomicrons in blood?
HDl comes along, donates E and CII, chylo binds to lpl breaks down to FA and glycerol (Fa to adipose, muscle, gly to liver)
70
what happens to vldl in blood?
hdl donates E and CII, lpl, Fa gly, HGT makes IDl to ldl
71
lpl is stimulated by:
CII and insulin
72
what does statin and cholestyramine do?
more ldl receptors
73
humans lack the enzyme to digest:
a- 1,3 and b 1,4
74
the glucose in oral dextran is from:
sucrose
75
starch is digested by:
a-amylase
76
on what from of carbs can be transmitted across epitheium?
monosaccharides
77
what receptors do monosaccharides go through in the lumen?
slgt1: glucose and galactose GUlt5: fructose
78
what receptor monosaccharides take to blood?
all glut5
79
sglt receptors couple what?
Na and glu/gal (cl and water follow)
80
glut5 is directly stim by
insulin
81
where does folate get carbons?
glycine
82
what does folate do with the carbon?
carries to syn purines and to B12
83
what is FH4
active form of folate, it accepts carbons can make purines (A and G), Pyrim (t) and gets trapped as methyl or B12 form
84
what happens to FH4 once it transfers methyl?
recycled except for in absence of B12 when it cant be recycled (folate trap)
85
what can folate deficiency cause?
inflammation` of tongue, mouth and ulcers
86
exampes of BCAA?
lucine isolucine valine
87
how are BCAA metabolized?
a-ketoacid dehydrogenase
88
what is maple surup urine?
decrease in a-ketoacid dehydrogenase causing buildup
89
what's treatment for maple syrup urine?
limit BCAA
90
what is classical PKU?
phenylalanine cant be transformed to tyrosine, so too much phe
91
how to treat PKU?
avoid phe and aspartame
92
what is alkaptonuria?
defect in homogentisate dioxygenase accumuation of homogentisate (back urine, eyes, ears, teeth)
93
what is homocystinuria?
defect in cystathionine synthase accumulates homosysyine in blood and urine
94
how to treat homocystinuria?
high dose Vit B6
95
what is a free radical?
molecule with one or more unpaired electrons
96
what is a NOXs?
NADPH oxidases, transfer electrons
97
what are mitochondrial ros?
electrons escape from ETC from complex 2 and 3, forming ROS
98
what is respiratory burst?
macrophages and neutrophils take in lots of O2 and release ROS to kill microorganisms
99
superoxide's are converted to H2O2 by:
superoxide dismutases
100
SOD requires:
zinc and copper
101
what is the primary thing needed for preventing lipid peroxidases
vit E
102
go over metabolism difference in diabetes 1 and 2