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CBFM Final > Questions To Redo From Practice Slides > Flashcards

Questions To Redo From Practice Slides Flashcards

1
Q

B12 deficiency is indicated by

A

High levels of methylmalomic acid and homocysteine

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2
Q

Folate deficiency is indicated by

A

High levels of of homocysteine

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3
Q

Homocysteine—-?—->cysteine

A

B6

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4
Q

What are and are NOT products of one-carbon receiver

A

Products: dTMP, serine, Purine, b12

NOT products: methylene

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5
Q

Bruising, poor wound healing and weak immune response indicates

A

Vitamin c deficiency

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6
Q

K2 source

A

Bacteria intestines

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7
Q

B6 source

A

Liver, fish, whole grains, nuts, legumes, eggs, yeast

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8
Q

B3 source

A

Liver, yeast, cereals, meat, legumes

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9
Q

B2 source

A

Liver

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10
Q

Copper deficiency leads to

A

Paleness
Decrease in the conversion of Fe2+ to Fe3+

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11
Q

What does Hypocalcemia lead to

A

Spontaneous, asynchronous, and involuntary contraction of skeletal muscle

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12
Q

What step of heme synthesis is B6 a cofactor of

A

Succinyl CoA + glycine —-B6 + ALA synthase—>ALA

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13
Q

Lead poisoning presents as

A

Fatigue, myalgia, clouded state, MICROCYTIC HYPOCHROMIC ANEMIA with BASOPHILIC STIPPLING of RBCs

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14
Q

What does lead poisoning cause an increase in

A

ALA - aminoluvulinic acid

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15
Q

How do you remember what ALAS1 and ALAS2 respond to and what they do

A

1 = “hehe” (Michael Jackson voice)
Means 1 responds to heme
1 is responsible for all tissues - think MJ is loved by allll

2= “ 2 eyyyyye” (deep voice)
Means 2 responds to Iron
2 is just for erythrocyte precursor

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16
Q

Increased CO2 would do what to the Hb graph

A

Shift it right

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17
Q

T from stabilized would do what to the Hb graph

A

Shift to the right

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18
Q

Decreasing pH would do what to the Hb graph

A

Shift it right

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19
Q

Increase in temperature would do what to Hb graph

A

Shift it right

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20
Q

It the Hb graph shifts to the right what should you think

A

Whatever is causing the shift is making it harder to uptake O2

Aka

Hb affinity for O2 has decreased

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21
Q

Deletion of 4 α chains

A

Barts syndrome

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22
Q

Deletion of 3 α chains

A

HbH
Aka
Hemoglobin H disease

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23
Q

What will the liver and the heart be doing in response to epinephrine

A

Liver will decrease glycolysis
Heart will INCREASE glycolysis

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24
Q

Why does cushings disease present as thin appendages and a big belly

A

Excess cortisol —> increase lipolysis to mobilize fats from the extremities and deposit them in the liver

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25
Q

GLUT4 is found ____ and is ____

A

Muscle and adipose tissue
Insulin dependent

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26
Q

Allosteric activator for PFK1

A

Fructose 2,6 bi-phosphate
And
AMP

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27
Q

What are the cofactors for PDH

A

B1 ( as TPP )
B2
B3
B5
LIPOIC acid

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28
Q

PDH is NOT regulated by ____ instead its _____

A

Regulated by insulin or glucagon

Instead its covlaently regulated by phosphorylation and Dephosphorylation g

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29
Q

What conditions will PDH operate under

A

AEROBIC ONLY

Bc PDH is the first step to make the TCA cycle go. The point of the TCA cycle is to produce NADH and FADH2 for the ETC. Since the ETC only works under aerobic conditions, the TCA follows in suit.

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30
Q

Does PPP require energy?

A

Yuh

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31
Q

Which ETC complex will be inhibited by an individual with a B2 deficiency

A

Complex 1

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32
Q

Which ETC complex will be inhibited by an individual with a malonate deficiency

A

Complex 2

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33
Q

Which ETC complex will be inhibited by an individual with a Fe deficiency

A

Complex 3
Think “free” like a toddler saying iron(Fe)

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34
Q

Which ETC complex will be inhibited by an individual with a Fe and Cu deficiency

A

Complex IV

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35
Q

Cyanide and carbon monoxide effect what ETC complex

A

IV

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36
Q

2,4 DNP effects

A

Overall: disrupts ETC proton gradient so that H= leaves the inter membrane space without generating any ATP

SO: you’re O2 consumption will be the same but ATP production will decrease.

It does this by:
In the inter membrane space DNP is protonated.
It can cross the inner membrane to the matrix.
Then in the matrix is drops of the H+ leaving DNP deprotonated.

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37
Q

If you don’t get O2 you can’t ____ which results in____

A

Undergo oxidative phosphorylation

ADP build up

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38
Q

Overall effects of TCA cycle in anaerobic conditions

A

Slows down
Less CO2 and NADH/FADH2 made

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39
Q

What is the first step of glycogen sythesis

A

Attachment of a glucose residue to the OH- group on Tyr-194 of glycogenin

Glycogenic is the protein responsible for kickstarting this step

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40
Q

Insulin (fed state) tends to ____

A

DEPHOSPHORYLATE

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41
Q

Glucagon/epinephrine (unfed/fasted state) tends to ____

A

PHOSPHORYLATE

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42
Q

How does Anderson disease present

A

Hepatosplenomegaly, cirrhosis, hypotonia, muscle weakness

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43
Q

What’s deficient in Andersen disease

A

Branching enzyme

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44
Q

What induces fructose 1,6 bisphosphatase and what path is this enzyme apart of

A

High glucagon

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45
Q

Saturated vs unsaturated FA

A

Sat= NO double bonds
Unsat= double bond ( think of my U, I I trick)

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46
Q

Path of ω3 fatty acids

A

Alpha linolenic acid —> eicosapentanoic —> docosahexaenoic —> anti-inflammatory

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47
Q

bile salt synthesis pathway story

A

Chloe “C7H” changed her name to Cloé A

She likes Tar and Gly

They got conjugated

So now they’re Bull Shit

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48
Q

What percent of bile is secreted and what percent is recycled

A

Secreted = 5% receyled = 95%

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49
Q

If there is a G6PD deficiency, the PPP will

A

Not be producing NADPH

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50
Q

Fatty acid synthase response to G6PD deficiency

A

FA synthase will decrease
Bc it needs NADPH and since the PPP is not making it, then FA synthase can’t work

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51
Q

To make FA you need

A

NADPH

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52
Q

To degrade FA you need

A

FAD and NAD+

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53
Q

Malate —-?—-> pyruvate

A

Malic enzyme

It makes NADPH

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54
Q

HMG CoA Reductase active for vs inactive form
What pathway is it in

A

Active = de phosphorylated
Inactive = phosphorylated

Cholesterol

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55
Q

β oxidation forms

A

1 Acetyl CoA
1 NADH
1 FADH2
14 carbon acyl CoA - this is 2 carbons shorter than the original

56
Q

Tangier Diesease effects ____ which in turn effects _____

A

HDL

VLDL and chylomicrons because the HDL cannot pass on C-11 and APO-E

57
Q

Hartnup disorder presentation

A

Lack of neutral AA - this includes tyrptophan

Tyrptophan def = Pellagra - 3Ds diarrhea, dermatitis, dementia

Think “hard up” - if someone is hard up they’re NOT neutral. They’re super excited. So they’re lacking neutral

58
Q

Histidine—-?—->hisamine

A

PLP - vitamin B6

59
Q

If ATP is low glutamate dehydrogenase makes what

A

α keto glutarate

60
Q

What does OTC Ornithine transcarbomolyase deficiency lead to and why

A

Increased orotic acid and increased NH4+
Bc carbomoyl phosphate starts leaking to the cytoplasm making orotic acid

61
Q

HGPRT stands for

A

Hypoxanthine guanine phosphoribosyltransferase

62
Q

How does lesch nyhan syndrome present

A

-gout, self mutilation, intellectual disability, disordered movement
-deficiency in HGPRT
-loss of purine salvage
-loss of purine salvage causes increases folate and/or B12 which leads to megaloblastic anemia. Which looks like hypersegmented neutrophils

63
Q

how would you treat dominant gain of function mutations

A

RNA interference where siRNA binds to mRNA and CRISPR/Cas9

When siRNA binds to mRNA mRNA is degraded

64
Q

What can adenoviruses cause

A

Massive immune responses

65
Q

To stop an alcoholic from drinking again you give them a drug that will

A

Inhibits ALDH(acetaldehyde dehydrogenase) which leads to an accumulation of acetaldehyde which results in hangover effects

66
Q

What does insulin do in skeletal muscle and adipose cells

A

De phosphorylates enzymes in pyruvate oxidation, lipolysis, glycogen synthesis, and glycogenolysis

67
Q

Adiponectin is _____ related to body fat

A

Inversely proportional

68
Q

When does the brain exclusively use ketone bodies as fuel

A

After 2-3 weeks of starvation

69
Q

After 4-5 days without food what would the liver be doing

A

Making glucose from AA

70
Q

What is the fate of even chain FA

A

Get metabolized to acetyl CoA and then go through the TCA to be made into ATP

71
Q

NADPH makes

A

Fatty acids!

72
Q

B12 deficiency presentation

A

Megaloblastic anemia
Glossitis
Motor and sensory anesthesia

73
Q

B6 deficiency causes

A

Alcoholic related deficiency

TB drug caused deficiency
-peripheral neuropathy
-stomatitis
-glossitis
-irritability
-psychiatric symptoms
-epileptic seizures
-Sideroblastic anemia

74
Q

Stationary and is a scavenger of free radicals

A

Vitamin E

75
Q

Too many raw egg whites cause a deficiency in this and what is it normally used for

A

Biotin
Protein purification

76
Q

Wilson disease

A

ATP7B gene mutation
Copper overload
Rings around cornea - key set fleisher rings

77
Q

Crigler Najjar syndrome

A

Increased unconjugated indirect hyperbilirubinemia due to DEFICIENCY of bilirubin glucuronyl transferase
Type 1 = totally deficient
Type 2 = less severe

Think “C”rigler, “D”efficiency- C is next to D in the alphabet

78
Q

Gilbert syndrome

A

Increased unconjugagted indirect hyperbilirubinemia due to mutation of glucuronyl transferase

79
Q

PCT - porphyria cutaneous tarda presentation

A

Chronic blistering
Tea colored urine
Elevation of transaminases

80
Q

PCT porphyria cutanea tarda mechanism

A

Deficiency in uroporphyrinogen decarboxylase (UROD -located in cytosol) which causes uroporphyrin accumulation

81
Q

If you block the ALA synthase step what builds and where

A

Succinyl CoA and glycine

82
Q

Methemoglobinemia (with auto recessive inheritance) mech and presentation

A

NADH cytochrome b5 reductase mutation

Chocolate blood

83
Q

Methemoglobinemia with auto dom mutation called __ where is it

A

Hemoglobin M
Heme binding pocket

84
Q

Balanced polymorphism happens where. Define it

A

Sickle cell trait

When someone is heterozygous for sickle cell.
Usually have no symptoms
Bonus it is selectively advantageous against malaria. THIS SPECIFICALLY IS CALLED - balanced polymorphism

85
Q

What indicates endogenous insulin production

A

C peptide

86
Q

GLUT4 does what in relation to glucose

A

It translocates to the cell membrane (muscle cell and adipose cell)
This can be triggered by exercise
The more GLUT4 on the cell acting as a receptor for glucose the less glucose in the blood

87
Q

A competetive inhibitor___

A

Raises the apparent Km for the substrate without changing the maximum rate

88
Q

Allosteric enzymes do not

A

Follow MM kinetics

89
Q

Where is glucokinase inducible

A

Liver and pancreas

90
Q

If you mess with PPP pathway what will in turn be messed up

A

FATTY ACID synthesis!!!!!
Cuz PPP makes NADPH
And NADPH is required for FA synthesis

91
Q

NADPH is used for

A

FA synthesis
And
Redox reactions involving glutathione

92
Q

What is wernicke Kordakis caused by

A

B1 deficiency

93
Q

B1 is a cofactor for what enzymes

A

Transketolase - moves 2c units in the PPP

Phyruvate dehydrogenase - converts pyruvate to acetyl CoA

Alpha ketogluturate dehydrogenase - generates NADH during the TCA for ETC

Branched chain AA Dehydrogenase - AA catabolism

94
Q

Pellegra is from ____ and presents as ___

A

Niacin B3 deficiency

Diarrhea, dermatitis, dementia

95
Q

Niacin helps make

A

NAD

And the reverse NADP

96
Q

Cori’s disease presentation

A

Fasting hypoglycemia, hepatomegaly, hypotonia, elevated creatinine kinase

Slide 91 in final review????

97
Q

Propionate to glucose path utilizes what vitamins

A

Biotin AND B12

98
Q

Which FA is essential for brain and eye development and is added to baby formula

A

Docosahexaeonic - ω3

99
Q

Butyric is ___ that causes ___ and is found in

A

Saturated FA

Growth arrest and apoptosis

Butter fat

100
Q

Myristic is ___ that causes ___ and is found in

A

Saturated FA

Rise in cholesterol

Palm kernel oil, nutmeg oil

101
Q

High yield unsat. FA

A

LA and LLAMA story.

Say it out loud for practice

102
Q

Acetyl CoA —?—>malonyl CoA

A

Acetyl CoA carboxylase

Biotin
B5 Pantothenic acid

103
Q

Carnitine is inhibited by

A

Malonyl CoA

104
Q

What process is malonyl CoA apart of

A

FA synthesis

Acetly CoA —Acetyl CoA carboxylase—>
malonyl CoA + acetyl CoA—-FAsynthse/NADPH—->
palmitate

105
Q

No food for 8 days, what are FA used for and what are triglycerides used for

A

FA - To make ketones!

Glycerol from the triglycerides provide live with carbon skeleton to make glucose

106
Q

Triglycerides provide ____ to the liver to use it as ____ to make ____

A

Glycerol

Carbon Skelton

Sugar

107
Q

5FU blocks

A

DTMP production

108
Q

Uric acid is the end product of

A

Purine degradation

109
Q

What path is fructose 2,6 bisphosphate in

A

Glycolysis

110
Q

PPP oxidative rxns
Are they reversible

A

G6P—G6PDH—> 6 phosphogluconate

6 phosphogluconate —-6PGD—> ribulose 5 phosphate

G6PDH stands for glucose 6 phosphate dehydrogenase and this step makes NADPH

6PGD stands for 6 phosphogluconate dehydrogenase and this step makes NADPH

NOT reversible

111
Q

PPP non oxidative rxns
Are they reversible

A

Transketolase (c2 unit) which is thiamine dependent

Transaldolase (c3 unit)

Yes it’s reversible

End products are 2 G3Ps, F6P

112
Q

Cholesterol phase 1 rxn

A

Acetyl CoA + acetyl CoA —HMG CoA synthase—>

HMG CoA —HMG CoA reductase+NADPH—>

Mevalonate

113
Q

Purine salvage

A

Adenine — APRT —> AMP

Hypoxanthine — HGPRT —> IMP

Guanine —HGPRT —> GMP

114
Q

Aminotranserase aspartate

A

Aspartate + αΚG —PLP B6——> OAA +glutamate

Asp gives NH3+ to glutamate

115
Q

aminotransferase Alanine

A

Alanine + αΚG ——PLP B6——> pyruvate +glutamate

Alanine gives NH3+ to glutamate

116
Q

Alanine can make

A

Pyruvate

117
Q

Aspartate can make

A

OAA

118
Q

Glutamate can make

A

AKG

119
Q

Glutamate —-?—-> aKG

A

Glutamate dehydrogenase
NADP+—->NADPH

120
Q

Sources of NADPH

A

1- glutamate -glutamate dehydrogenase-> aKG
2- G6P -G6PDH-> 6PG -6PGD-> ribulose
3-malate —malic enzyme —> pyruvate

121
Q

IREs in 5’ UTR

A

Ferritin, ALAS2

122
Q

____ translation of IRE in 5’ UTR when iron is low

A

Decreased

123
Q

IREs in 3’ UTR

A

Transferrin receptor and DMT1

124
Q

Transferrin receptor and DMT1 mRNAs are ____ when Iron levels are high.

Therefore. They’ll be ___when iron levels are low. This ____ helps bring ____

A

Unstable

Stable
Increased, more iron in

125
Q

-ΔG substrate to product ratio
Keq =

___ of energy

A

Product>substrate
Keq>1
Loss of energy

126
Q

Methotrexate inhibits

A

DHF
So dTMP cannot form

127
Q

Purine degradation leads to

A

Uric acid formation
No energy is made

128
Q

Key in prolonged fasting

A

Muscles decrease their use of KB. The brain starts to use a lot of KB

129
Q

Normal serum albumin levels
High levels of blood ammonia - muscle wasting
Low Creatinine height index

A

Marasmus

130
Q

Chronic kidney disease

A

Cachexia pt

131
Q

Wacky BUN indicates

A

Wacky kidney

132
Q

Anorexia pt have

A

Hypoalbuminemia

133
Q

Total caloric insufficiency

A

Marasmus

134
Q

Protein deprivation

A

Kwashiorkor

135
Q

Unconjucated present?
Can’t transport conjugated?
Lowered expression of bilirubin glucuronyl transferase

A

Crigler - “d”ef, unconjucated. can’t die uncut
Dubin - dubin is a con for metals, rubies, pears (MRP2)
Gilbert- the gilberts are common(common disease) but have lowered expression since BGT (big god took) their dad

CBFM Final (18 decks)

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