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Biochemistry > CHAP 8-18 > Flashcards

CHAP 8-18 Flashcards

1
Q

Quantos são os AA hidrofóbicos?

A

9

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2
Q

Quais são os AA hidrofóbicos?

A 
1- Glycine (Gly)
2- Alanine (Ala)
3- Valine (Val)
4- Leucine (Leu)
5- Isoleucine (Ile)
6- Proline (Pro)
7- Phnylalanine (Phe)
8- Tyrosine (Tyr)
9- Tryptophan (Trp)
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3
Q

RESPONDA RÁPIDO

Phenylalanine and Tyrosine são precursores da:
1 resposta

A

Catecolaminas

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4
Q

RESPONDA RÁPIDO

Tryptophan é precursor das:
2 respostas

A

1- serotonin

2- Niacin (Vit B3)

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5
Q

RESPONDA RÁPIDO

Valine, Leucine and Isoleucine são AA …….. chain, cujo a ausencia da enzima que faz o seu metabolismo causa………

A

Branched/ maple syrup urine disease

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6
Q

Maple syrup urine disease é causado pelo matabolismo deficiente de quais AA?

A

Valine, Leucine and Isoleucine

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7
Q

GLYCINE (Gly) is the most common AA in …….

A

Collagen

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8
Q

Alanine está relacionado a …………… Que converte a alanina em …………… com auxílio da enzima……. e da vitamina……….

A

Starvation/ piruvate/ alanine transaminase (ALT)/ B6

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9
Q

Proline is hydroxylated by………. cujo reação necessita de………… com o objetivo de fazer as ligacoes de………..
A deficiência dessa hidrolizacao causa………

A

Prolyl hydroxylase/ vit C/ Hydrogen/ scurvy

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10
Q

Phenylalanine é um AA natural ou essencial?

A

Essencial

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11
Q

Phenylalanine é convertida em ………. através da enzima……………….. e do cofator………. A deficiencia de um desses dois causa a doença……………….

A

Tyrosine/ phenylalanine hydroxylase/ THB/ phenylketonuria

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12
Q

A phenylketonuria é causada pela deficiência de ………

2 respostas

A

Enzima phenylalanine hydroxylase e cofator THB

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13
Q

Tyrosine é convertida em:
1-
2-
3-

A

1- Melanina
2- Dopamina (catecolaminas)
3- hormônios tireoidianos

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14
Q

Além de ser convertida em melanine, catecolamines e hormônios tiroideanos, a Tyrosine também target……… receptors. Presentes na ………., …………., e …………… Cuja presença pode se relacionar com ……………

A

Tyrosine Kinases/ insulin, growth factots, cytokines/ cancer

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15
Q

Doença na qual o tryptophan não pode ser reabsorvido no tubulo proximal é………. Que se manifesta como ……….

A

Hartnup disease/ pelagra

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16
Q

Carninoid no estômago libera muita…….. Diminuindo a concentração do AA……….. e da Vitamina …………, causando sintomas semelhantes a ……………

A

Serotonin/ Tryptophan/ B3/ Pelagra (3D- demencia, dermatite, diarreia)

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17
Q

Os aminoácidos POSITIVOS sao………., ………….. e …………….. que tem o ph …………..

A

Lysine (Lys)/ Arginine (Arg)/ Histidine (His) - weakly +/ Basic

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18
Q

Os aminoácidos NEGATIVOS sao………. e …………….. que tem o ph …………..

A

Aspartate (Asp)/ Glutamate (Glu)/ Acid

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19
Q

Arginine and Lysine are part of the nucleus by being the primary AA in ………..

A

Histones

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20
Q

Lysine is hydroxylated by………. cujo reação necessita de………… com o objetivo de fazer as ligacoes de………..
A deficiência dessa hidrolizacao causa………

A

Lysyl hydroxylase/ vit C/ Hydrogen/ scurvy

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21
Q

Arginine is produced during the …………. and form ………..::

A

Urea cycle/ nitric oxide

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22
Q

Wich AA works as a Buffer base and can be converted to Histamine?

A

Histidine (His)

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23
Q

Wich AA takes NH3 into the urea cycle?

A

Aspartate (Asp)

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24
Q

Which AA works as an excitatory neurotransmissor and can turn into a inhibitory neurotransmissor named………?

A

Glutamate/ GABA

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25
Q

Site of the O-glycosylation in the Golgi is ………. and ………..

A

Serine and Threonine

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26
Q

Reduced form of Cysteine is part of …………… Important to stop ………..

A

Glutathione/ Free radicals

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27
Q

G6PD deficiency is a result of a problem on the AA…………. That decrease ………… and increase ………… that attack the …………. leading to …………

A

Cysteine (Cys)/ Glutathione/ free radicals/ red blood cells/ hemolisis

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28
Q

Heinz bodies are ……………. formed by …………… when glutathione is gone

A

Deformed Hb/ free radicals

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29
Q

In the AA…………the methyl (CH3) gruop is used to make …………. and …..…… making ..………

A

Methionine (Met)/ mRNA cap/ epinephrine/ homocystein

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30
Q

Homocystein can be converted back to …………… by using ………… and …………

A

Methionine / Vit B12/ Folic Acid

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31
Q

Site of the N-glycosylation …………. in the…………

A

Aspargine (Asn)/ ER

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32
Q

What is the AA that receives NH3 in the blood to prevent ph changes during ……… breaksdown?

A

Glutamine (Gln) / Protein

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33
Q

What are the essential AA that never become Glucose

2 respostas

A

Leucine (Leu) and Lysine (Lys)

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34
Q

AA thats is part of 33% of collagen

A

Glycine

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35
Q

Most commonly mutated AA in collagen

A

Glycine

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36
Q

Se o DELTA G de uma reaçao é NEGATIVO, ela acontece…………… Então mais ………….. são formados

A

Espontaneamente/ produtos

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37
Q

Se o DELTA G de uma reaçao é POSITIVO, ela acontece…………… Então mais ………….. são formados

A

Com consumo de energia/ substrato

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38
Q

As enzimas são capazes de alterar a quantidade de energia necessária ou liberada em uma reação?

A

No

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39
Q

Vmax depende da quantidade de …………

A

Enzymes

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40
Q

Km é a quantidade de ……. necessaria para atingir ………. da …………

A

Substrato/ metade/ vmax

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41
Q

Km representa a ………. da enzima para o ………..

A

Afinidade/ substrato

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42
Q

Low Km …….. affinity

A

Higher

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43
Q

Arginine is an essential AA during ……….. and ………

A

Growth / positive nitrogen balance

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44
Q

In the Lineweaver-Burk Equation the x-axis interception reffers to ……… and the y-axis interception reffers to………

A

-1/km (affinity) / 1/Vmax (vmax)

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45
Q

Competitive antagonists bind to ……… site in the same receptor

A

Same

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46
Q

Non-competitive antagonists bind to ……… site on the same receptor

A

Different

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47
Q

Competitive antagonism ……..Vmax …………Km

A

Don’t change/ increase

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48
Q

Non-Competitive antagonism ……..Vmax …………Km

A

Decrease/ don’t change

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49
Q

Cooperative enzymes have ……… sites for different ……… and ………

A

Multiple/ activators/ inhibitors

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50
Q

On cooperative enzymes kinetics (PFK1, activators ……… affinity, ……… Km, in the presence of ………

A

Increase/ decrease/ ADP

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51
Q

On cooperative enzymes kinetics (PFK1, inhibitors……… affinity, ……… Km, in the presence of ………

A

Decrease/ increase/ ATP

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52
Q

Which AA has a thiol (-S) group?

A

Cysteine

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53
Q

Protein kinase is an enzyme that ……… other proteins, changing their ………

A

Phosphorilates/ activity

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54
Q

Protein Gs stimulates ………(enzyme inside the cell), that increases ………, made of………, that releases ………

A

Adenyl cyclase/ cAMP/ ATP/ protein Kinase A

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55
Q

The Gi coupled receptors are: (3 answers)

A

MAD2 (alpha 2, M2, Dopamine 2)

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56
Q

Which AA is essential only during growth and positive nitrogen balance?

A

Arginine

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57
Q

Gq protein activates ………that increases ……… and ……… Increasing………

A

Phospholipase C/ IP3/ DAG/ protein Kinase C

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58
Q

The second messenger IP3 increases ……… to release ………

A

Calcium/ protein kinase C

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59
Q

ANF binds to its receptor, activating ………, that increase ………, made of ………, releasing ………

A

Guanyl cyclase/ cGMP/ GTP/ protein kinase G

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60
Q

NO ……… the membrane, and activates ………that increase ………, made of ………, releasing ………

A

Pass through/ soluble guanyl cyclase/ cGMP/ GTP/ protein kinase G

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61
Q

Janus kinase (JAK) =…………. for example………

A

Tyrosine Kinase pathway (not in the membrane it self- like insulin receptor and growth factor) / growth hormone

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62
Q

Insulin receptors are………
When they are activated they attract..…… that mainly activate three different proteins: ……… at the liver, ……… at adipose and skeletal tissue, ……… that change gene expression

A

Tyrosine kinase / SH2 proteins/ protein phosphatase 1/ PI3- kinase/ p21 ras Cytoplasms G protein

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63
Q

Os metabólitos do etanol se ligam a vitamina ……… acabando o seu estoque. O que gera a doença ………

A

B1/ wernicke (ataxia, nistagmo)-korsakoff (confabulation, psychosis, memory problem)

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64
Q

Qual enzima é dependente APENAS da Vit B1 (Thiamine) para funcionar?
Ela está mais relacionada com a deficiência dessa enzima que gera……

A

Transketolase/ wernicke-korsakoff

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65
Q

Quais sao as enzimas que requerem B1, B2, B3, B5 e lipoic acid? ………, ……… and ………

A

Pyruvate dehydrogenase/ alfa-ketoglutarate dehydrogenase/ branched chain ketoacid dehydrogenase

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66
Q

No tecido adiposo e musculo, a insulina ativa o ………, cuja acao é aumentar o ……… na membrana plasmática

A

PI-3 kinase / GLUT4

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67
Q

No figado, a insulina aumenta a ………, responsável pela……… das enzimas

A

Protein phosphatase-1/ dephosphorylation

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68
Q

A insulina é capaz de modular o gene expression no nucleo atraves da ……

A

p21ras Gprotein

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69
Q

Glucagon activates PKA, that phosphorilate ………, ……… it’s activity and also phosphorilate ………, ……… it’s activity

A

Glycogen phosphorylase/ increasing / glycogen synthase/ decreasing

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70
Q

Insulin activates protein phosphatase 1, that dephosphorilate ………, ……… it’s activity and also phosphorilate ………, ……… it’s activity

A

Glycogen phosphorylase/ decreasing / glycogen synthase/ increasing

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71
Q

Cholera and E.coli fazem o ADP ribolsylation em…………, increasing …………

A

Gs protein/ cAMP and PKA

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72
Q

Pertusis faze o ADP ribolsylation em…………, increasing …………

A

Gi protein/ cAMP and PKA

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73
Q

ADP rybosilation of Gs ………, leading to ………cAMP

ADP rybosilation of Gi ………, leading to ………cAMP

A

Stimulates/ more/ inhibits/ more

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74
Q

What toxins make the ADP ribosylation? (5 bacterias)

A

Pseudominos/ diphtheria/ cholera/ E coli/ pertussis

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75
Q

What is the cellular target and effect of pseudomonas and diphteria?

A

eEF2 (eukaryotic elongation factor 2) / inhibit translation

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76
Q

What is the cellular target and effect of cholera and e coli?

A

Gs/ increase c AMP and PKA activity

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77
Q

What is the cellular target and effect of pertusis?

A

Gi/ increase c AMP and PKA activity

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78
Q

Where the toxin get ADP ribose group?

A

NADH

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79
Q

QUal enzima é mais relacionada com a deficiência de Thiamina (B1?)

A

Transketolase

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80
Q

Quais enzimas necessitam das vitaminas B1,B2,B3,B5 e lipoic acid para funcionar?

A

Pyruvate dehydrogenase
Alfa ketoglutarate dehydrogenase
Branched chain ketoacid dehydrogenase

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81
Q

What are the symptoms of Thiamine deficiency?

A

Wernicke (ataxia, nystagmus)
Korsakoff (psycosis, memory issues)
Wet Beri-beri (cardiac failure)
Dry beri-beri (peripheral neuropathy)

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82
Q

Viramin B2 is named

A

Riboflavin

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83
Q

A vitamina B2 está relacionado a ………, gerando parte do ………, capaz de produzir ………

A

Oxidative phosphorylation (redox)/ FADH2/ 2 ATP

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84
Q

Os sintomas relacionados a deficiência de vitamina B2 são (3 sintomas)

A
  • corneal neovascularization
  • cheilosis and stomatitis
  • magenta coloured tongue
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85
Q

A vitamina B3 está relacionado a ………, gerando parte do ………, capaz de produzir ………

A

Oxidative phosphorylation (redox)/ NADH e NADPH/ 3 ATP

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86
Q

NADH é responsável por ………, while NADPH é responsável por ………, ……… and ………

A

Oxidative phosphorylation (redox)/ fatty acid synthesis/ immune response/ glutathione regeneration

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87
Q

Deficiência de vitamina B3 pode ser causada devido ……… e ………

A

Dieta baseada principalmente em corn (low in tryptophan) / Hartnup disease

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88
Q

Vitamin B6 is named

A

Piridoxine

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89
Q

Piridoxine is used in the ……… by ………

A

Liver/ transaminases

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90
Q

Piridoxine is responsable for …… synthesis. It’s deficiency causes ………

A

Heme / sideroblastic anemia

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91
Q

B6 deficiency is mainly caused by…………

A

isoniazid therapy

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92
Q

B6 deficiency can cause (3 sintomas)

A

Sideroblastic anemia/ cheilosis and stomatitis/ homocysteinemia (b6 is needed to metabolize homocysteine)

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93
Q

Biotin (b7) pathway is VOMIT, which means

A

Valine, odd carbon fatty acids, methionine, isoleucine, threonine

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94
Q

Biotin deficiency is rare, and it’s usually due to ………, leading to symptoms like (3 symptoms)

A

Consumption of raw egg/ alopecia/ bowel inflammation/ muscle pain

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95
Q

Folic Acid is part of the pathways of ……… and ……… synthesis, and ……… recycling

A

Purines/ pyrimidines (DNA/RNA)/ methionine

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96
Q

Acid Folic deficiency is more common in ………, ……… and ………

A

Alcoholism/ pregnancy/ hemodialysis

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97
Q

Deficiency in Folic Acid can cause ………, ……… and ……… in fetus

A

Megaloblastic anemia/ homocystinemia/ neural tube defects

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98
Q

Medicines that are nhibitors of dehydrofolate reductase ( convertion of folic acid into folate) are ………, ……… and ………. Causing ………

A

Methotrexate/ trimethoprim/ pyrimethamine / megaloblastic anemia

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99
Q 
Causes of deficiency of Cyanocobamin (B12): 
1- 
2- 
3-
4-
5-
6-
A 
1- pernicious anemia
2- aging with poor nutrition
3- bacterial over growth of ileum
4- resection of terminal ileum in Chron
5- chronic pancreatitis 
6- vegan (rare)
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100
Q

Vit B12 deficiency cause:
1-
2-
3-

A

1- megaloblastic anemia
2- homocystein
3- progressive peripheral neuropathy

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101
Q

Ascorbate deficiency cant hydroxilase …… and ………. Leading to a problem in ………, causing ………

A

Proline / lysine/ collagen/ scurvy

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102
Q

Ascorbate deficiency can’t readily absorb ……, leading to ………

A

Iron/ anemia

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103
Q

If the simptoms are scurvy-like, but there are plenty of Vitamin C, it is ………, due to deficiency of ………

A

Ehler-Danlos/ hydroxilase enzymes

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104
Q

High dose Niacin can be used to treat ……

A

Hyperlipidemia

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105
Q

Vitamins A and D work through ……… similar to those for lipid-soluble hormones

A

Enhancer mechanisms

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106
Q

Lipid soluble vitamins …, … and … are stored in the liver, while lipid soluble vitamin … is stored in adipose tiasue

A

D,A,K/ E

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107
Q

Vitamin D is named ……

A

Cholecalciferol

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108
Q

Vitamin D, in response to hypocalcemia, helps normalize ………

A

serum calcium levels

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109
Q

3 types of vitamin A

A
  • Retinol (growth regulator in the epithelium)
  • Retinoic acid (growth regulator in the epithelium)
  • Retinal (rods and cones)
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110
Q

Vitamin A(carotene) retinol and retinoic acid are ………, while retinal is important in………

A

Growth resulators in the epithelium/ rod and cones

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111
Q

Vitamin K is responsable for ……… of ……….in many Ca binding proteins.

A

Carboxylation/ glutamic acid residues

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112
Q

Which enzyme is important for carboxylation of glutamic acid in many Ca binding proteins

A

Vitamin K

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113
Q

Vitamin E is an

A

Antioxidant in lipid phases

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114
Q

7-dehydrocholesterol produces ……… using UV light

A

Cholecalferol (Vitamin D3)

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115
Q

In the liver, the cholecalciferol is transformed in ………, by the enzime ………

A

25-hydroxycholecalciferol/ 25-hydroxilase

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116
Q

No tubulo proximal, 25-hydroxycholecalciferol is transformed into ………, by the enzyme ……… That is released in response to ……

A

1,25-dihydroxycholecalciferol/ 1alfa hydroxilase/ PTH

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117
Q

Alguns pacientes nao sao capazes de produzir a 1,25-DHCC, necessitando de suplementação desse hormônio devido a: (3 respostas)

A

1- end stage renal disease
2- sd de fanconi
3- genetic deficiency of 1 alfa hydroxylase

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118
Q

Vitamin D toxicity symptoms are: ……, ……, …… and …… Prolonged hypercalcemia can impair ……

A

Hypercalcemia, polyuria, polydipsia, nocturia/ renal function

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119
Q

Deficiency of Vitamin D in kids cause ……. And in adults cause……

A

Rickets/ osteomalacia

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120
Q

Vitamin D deficiency can be due to (3 respostas)

A
  • end stage renal disease
  • insufficient sublight
  • insufficient fortified food (milk)
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121
Q

Vitamin A deficiency can cause (4 answers)

A
  • night blindness
  • xerophtalmia
  • bitot spots
  • alopecia
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122
Q

Symptoms of vitamin A toxicity (6 answers)

A
  • brittle nails
  • dry skin
  • teretogenic in pregnancy
  • excessive sweating
  • diarrhea
  • hepatosplenomegaly
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123
Q

Vitamin K is required to introduce … binding site on several … dependent proteins. The modification which introduces the … binding site is ………of glutamyl residues

A

Ca/ Ca/ Ca/ gama carboxylation

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124
Q

Proteins undergoing Vitamin K dependent carboxylation are: (6 answers)

A
  • coagulation factors: 2,7,9,10

- anticoagulant proteins C and S

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125
Q

Vitamin K deficiency is related to ; (4 answers)

A

1- fat malabsorption
2- long term antibiotics
3- breast fed newnorns (no flora to produce vit k, breast milk is low in vit k)
4- infant whose mothers was taking anticonvulsant during pregnancy

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126
Q

After been used, Vitamin K is oxidized, becoming unsuable. The enzyme that recycle Vitamin K is ……… That is inhibited by ………

A

Vitamin K Epoxide Reductase/ warfarin

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127
Q

Vitamin E deficiency can lead to (5 answers)

A
  • hemolisis
  • acanthosis
  • ataxia
  • Peripheral neuropathy
  • retinitis pigmentosa
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128
Q

Hemorrhage and necrosis in the mammillary bodies and the gray matter reffers to which vitamin deficiency?

A

Thiamine (Vit B1) - korsakoff

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129
Q

Which vitamin deficiency is related to elevated methylmalonic acid levels?

A

Vitamin B12

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130
Q

Glucose comes inside the liver trough GLUT 2, and when insulin is activated, it gets traped inside the liver by ………… enzyme

A

Glucokinase

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131
Q

When insulins is active, the enzyme that converts glucose to glycogen is ………

A

Glycogen synthase

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132
Q

In order to store energy, insulin also makes fatty acid. However to do so it needs increase glycolysis, by converting more glucose in to pyruvate stimulating the enzymes ……… and ………

A

Pyruvate kinase, PFK-2

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133
Q

In order to store energy, insulin also makes fatty acid. However to do so, it needs increase glycolysis, by converting more glucose in to pyruvate and then pyruvate into acetyl CoA, by stimulating the enzyme ………

A

Pyruvate dehydrogenase

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134
Q

In order to store energy, insulin also makes fatty acid. However to do so, it needs increase glycolysis, by converting more glucose in to pyruvate, then pyruvate into acetyl CoA, and acetyl CoA into Fatty Acid by stimulating the enzymes ……… and ………… The fatty acid will then be taken to the adipose tissue by

A

Acetyl CoA carboxylase/ fatty acid synthase/ VLDL

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135
Q

In the adipose tissue, the fatty acid is transported from the VLDL to the cell using the ………., that is stimulated by the insulin.
In the adipose tissue, insulin also increase the uptake of glucose by increasing the expression of ………

A

Lipoprotein Lipase/ GLUT 4

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136
Q

Muscles can increase GLUT 4 expression during exercise through ……..

A

AMP kinase pathway

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137
Q

In the post-absorptive statge, Glucagon breaks Glycogen (glycogenolysis) using the enzyme ……

A

Glycogen phosphorylase

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138
Q

…… is the primary glucose source for the first 12 hours post-meal. ……… is the primary glucose source for after 12 hours post-meal.

A

Glycogen/ Gluconeogenesis

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139
Q

Cell that uses glycolysis as the only energy source

A

Red blood cells

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140
Q

GLUT 1 and GLUT 3 have ……… affinity to glucose. At normal glucose blood concentration they funtion on …… order

A

High/ zero

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141
Q

GLUT 2 is a …… affinity transporter. In the …… it captures the excess of glucose to ……… and in the …… it serves as a glucose sensor for ……

A

Low/ hepatocytes/ store/ pancreas/ insulin release

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142
Q

The rate of glucose transport in GLUT 4 is increased by ……

A

Insulin

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143
Q

In the pancreas,Glucose gets inside the cell through ……… and get traped insidide the cell through ……… Then it pass through Glycolysis and TCA cycle, forming …… This closes the ………channel, ……… the membrane, wich opens …… channel, that releases ……

A

GLUT 2/ glucokinase/ ATP/ Katp/ depolarising/ Ca channel/ insuline

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144
Q

Sulfonylureas block …… channels, depolarising the cell and releasing ……

A

K/ insulin

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145
Q

Thiazide and Diazoxide keeps …… channel ……, ……… insulin secretion

A

K/ open/ decreasing

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146
Q

Glycolysis converts glucose into 2 …… using 2 ………… reaction and 1 …… reaction

A

Pyruvate/ substrate-level phosphorilylation/ oxidation

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147
Q

During glycolysis, the three most important enzymes are (4 answers)

A
  • hexokinase /glucokinase (liver)
  • PFK-1
  • pyruvate Kinase
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148
Q

During glycolysis, a defect on the enzyme ……… can lead to ………., increased ………, no ……….
This is the second most common cause of……..

A

Kinase/ hemolytic anemia/ BPG/ heinz bodies/ hemolytic anemia

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149
Q

The rate-limiting enzyme during glycolysis and the main control point is (1 answer)

A

PFK-1

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150
Q

In the liver, insulin stimulate ……, that stimulate ……

A

PFK-2/ PFK-1

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151
Q

Galactose metabolism happens is the ..…, …… and other tissues

A

Liver/ brain

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152
Q

Galactosemia is an defficiency in two enzymes:

A

Galactokinase/ Galactose -1-P uridyl transferase

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153
Q

A more mild galatosemia happens in the defficiency of …… causing ……

A

Galactokinase/ cataracts early in life

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154
Q

A more severe galatosemia happens in the defficiency of …… causing …… (5 answers)

A 
Galactose -1-P uridyl transferase/ 
1- cataracts life
2- vomiting, diarrhea
3- letargy
4- liver demage, hyperbilirubinemia
5- mental retardation
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155
Q

In the well fed state, galactose can enter ……… or contribute to ……… storage

A

Glycolysis/ glycogen

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156
Q

Administration of galactose during hypoglycemia induces an increase in blood ………

A

Glucose

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157
Q

If galactose acumulates, it goes to the ……… and get transfromed into ……… with the enzyme ………. Causing ………

A

Lens/ galactitol/ aldose reductase/ cataracts

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158
Q

Early cataracts can be caused by ……… and ……… In the diabetics, the excess of glucose gets converted to ………by the enzyme ………

A

Galactosemia/ Diabetis/ sorbitol/ aldose reductase

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159
Q

Benign fructokinase deficiency is ……………

A

Essential fructosuria

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160
Q

Fructose metabolism happens in the ……… and ………

A

Liver/ Kidney

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161
Q

A more severe enzyme deficiency during fructose metabolism is ………, also called ………, causing symptoms like ………(5 answers), when solids are added to diet

A

Adolase B deficiency/ hereditary fructose intolerance/
1- letargy, vomiting
2- liver demage, hyperbilirubinemia
3- hypoglycemia
4- hyperuricemia, latic acidosis
5- Renal Proximal Tubule deffect (Fanconi)

162
Q

Pyruvate from aerobic glycolysis enters the ……… , where its converted to ……… for entry into the ……… cycle, If ATP is needed, or for ……… if sufficient ATP is present

A

Mitochondria/ acetyl-CoA/ citric acid/ fatty acid synthesis

163
Q

Pyruvate Dehydrogenase (PDH) in the liver is activated by ………, he brain and nerves the enzyme ………to hormones

A

Insulin/ does not respond

164
Q

Outside the liver, the pyruvate dehydrogenase is stimulated by ………, and inhibited by ………, ………, and ………

A

Serum Calcium/ ATP/ NADH/ Acetyl-CoA

165
Q

Citric acid cycle/krebs cycle/tricarboxylic acid cycle happens in the

A

Mitochondria

166
Q

In the citric cycle, all the enzymes are in the matrix of the mitochondria, except ……, which is in the ……

A

Succinate dehydrogenase/ inner membrane

167
Q

The enzyme that makes the major control of the Kreb Cycle is …… This enzyme is inhibited by …… and ……, and is activated by ……

A

Isocitrate dehydrogenase/ ATP/ NADH/ ADP

168
Q

What enzyme in the Kreb Cycle catalyses a substrate level phosphorylation of ……. to …….:

A

Succinyl-CoA synthetse/ GDP/GTP

169
Q

The enzyme …… is on the inner mitochondrial membrane, where it also function as ………. of the ETC

A

Succinate dehydrogenase/ Complex II

170
Q

When there’s too much energy made up……may leave the mitochondria through …….. to deliver …… into the cytoplasm for ……….

A

Citrate / citrate shuttle/ Acetyl-CoA/ fatty acid synthesis

171
Q

In the cytoplasm, citrate can inhibit …… by inhibiting the enzyme ……, and stimulate ……….

A

Glycolysis/ PFK-1/ fatty acid synthesis

172
Q

The only dehydrogenase that only needs B2 is ……..

A

Succinate dehydrogenase

173
Q

In the TCA cycle, all the enzymes are in the mitochondria matrix, except …….., that is located in the ……..

A

Succinate dehydrogenase / inner membrane

174
Q

OIL and RIG means

A

Oxidation is Loss of Electrons

Reduction is Gaing of Electrons

175
Q

In the electron transport chain, the Complex I enzyme is the ………, that oxidize ……… This pathway can be stoped by ………. and ………..

A

NADH dehydrogenase/ NADH/ barbiturates/ rotenone (an isecticide)

176
Q

In the electron transport chain, FADH2 pass trough the complex ……., and can be stoped by…….

A

Coenzyme Q (ubiquinone)/ doxorubicin

177
Q

In the ETC, the complex III is inhibited by ……..

A

Antimycin

178
Q

In the ETC, the complex IV can be stoped by ……. and …….. Which can be found in …….. and ………..

A

Cyanide/ CO/ house firework with plastic/ nitroprusside

179
Q

The Complex V ( F0-F1) can be stopped by ……..

A

Oligomycin

180
Q

Uncouplers …….., ….. and …….., pass the protons through the membrane, leading to lost of heat without ATP synthesis

A

Dinitrophenol (2,4 DNP)/ aspirin/ thermogenin

181
Q

Most of the poisons of ETC ……. the ETC, resulting in …….. ATP and ……. use of O2. While uncouplers ……. the ETC, resulting in …….. ATP and ……. use of O2

A

Stops/ no/ less/ increases/ no/ more

182
Q

Cyanide poisoning treatment is made in …. steps, first step aims to ……., second step aims to ………., third step aims to ……….

A

3/ trap cyanide in the blood/ make a safe metabolite/ fix metHb

183
Q

The first step of cyanide poisoning treatment aims to trap the cyanide in the blood using …….., that transforms the ……. to ………

A

Nitrite/ HbFe2+/ HbFe3+ (methemoglobin)

184
Q

The second step of cyanide poisoning treatment aims to make a safe metabolism by using …….

A

Thiosulfate

185
Q

The third step of cyanide poisoning treatment aims to fix the methemoglobin by using………..

A

Methylene

186
Q

Cyanide poisoning can also be treated using ……

A

Vitamin B 12

187
Q

Succinyl-CoA is a substrate used in the …… synthesis

A

Heme

188
Q

When Oxigen is partially reduced, unstable products called ……….. are formed

A

Reactive oxygen species (ROS)

189
Q

What are the Reactive Oxygen Species (ROS)?

A
  • superoxide (O2-)
  • hydrogen peroxide (H2O2)
  • Hydroxyl radical (OH)
190
Q

Defense against ROS accumulation are very important in highly aerobic tissue and erythrocytes, because superoxide is generated by spontaneous dissociation of oxygen and Hb. This produces …….. and ………., leading to ……..

A

Methemoglobin/ superoxide/ hemolysis

191
Q

The three enzymes that make substrate level phosphorylation are …, …. and …..

A

Phosphoglycerate kinase/ pyruvate kinase/ succinil coa synthetase

192
Q

…… is an enzyme in the TCA cycle that instead of B3, it requires just B2

A

Succinate dehydrogenase (complex II)

193
Q

The first step of the ETC is the Complex I, named … which can be poisoned by …. and …

A

NADH dehydrogenase/ barbiturates / rotenone (pesticide)

194
Q

In the ETC, FADH2 skips complex.. and go straight to the ……… step, wich can be inhibited by……

A

I / Coenzyme Q(ubiquinone)/ doxorubicin

195
Q

Glycogen is stored in the cells in the branched form because is more …. and is …… to cut

A

Soluble / faster

196
Q

Glycogen is made using the enzymes …. and …., that are stimulated by the …

A

Glycogen synthase/ branching enzyme / insulin

197
Q

In glycogen synthesis, the enzyme glycogen synthase makes the …. bonds, while the branching enzyme makes the ….. bonds

A

1,4 linear / 1,6 branched

198
Q

Glycogen can be broken down using the enzymes …. and …., that are stimulated by the … (in the liver), … (in muscle and liver), … (in the muscle)

A

Glycogen phosphorylase / debranching enzyme/ glucagon/ epinephrin/ AMP

199
Q

In glycogen break down, the enzyme glycogen phosphorylase breaks the …. bonds, while the debranching enzyme breaks the ….. bonds

A

1,4 linear / 1,6 branched

200
Q

After glycogen breaks down, glucose can be released only in the … using the enzyme ….

A

Liver / glucose 6- phosphatase

201
Q

The glycogen storage disease type I is named …….. or ………, and it’s a deficiency of the enzyme ……. Leading to accumulation of ……. It’s symptoms are …, …., ….., …. etc

A

Glucose -6- phosphatase Deficiency/ von Gierke Disease/ glucose 6 phosphatase/ glucose 6P/ severe hypoglycaemia/ lactic acidosis/ hyperuricemia/ hyperlipidemia

202
Q

The Glycogen Storage Disease Type II named …., is characterised by a deficiency in the …. enzyme, causing the accumulation of ……., leading to ….. , …….. and death by ..yo

A

Pompe Disease/ Lysossomal alfa 1,4-glucosidase/ glycogen like material in inclusion bodies/ cardiomegaly/ muscle weakness/ 2

203
Q

The Glycogen Storage Disease Type III named …., is characterised by a deficiency in the …. enzyme, leading to ….. and ……..
In the glycogen structure, we see small fragments of of branches left on the glycogen

A

Cori disease/ glycogen debranching enzyme/ mild hypoglycaemia/ liver enlargement.

204
Q

The Glycogen Storage Disease Type IV named …., is characterised by a deficiency in the …. enzyme, leading to glycogen structure ….. with ……… It causes symptoms like ……. and death by … yo

A

Andersen/ branching / long/ few branches/ cirrhosis/ 2

205
Q

The Glycogen Storage Disease Type V named …., is characterised by a deficiency in the …. enzyme, leading to ….. , …….. and ……..

A

McArdle/ Muscle Glycogen Phosphorylase (myophosphorylase)/myoglobinuria/ muscle cramps and weakness on exercise

206
Q

The Glycogen Storage Disease Type VI named …., is characterised by a deficiency in the …. enzyme, leading to ….. , ……. and ……..

A

Hers Disease/ hepatic glycogen phosphorylase/ mild hypoglycaemia/ hepatomegaly/ cirrhosis

207
Q

The three important substrates for gluconeogenesis are:
1- …., from …..
2- …., from …..
3- …., from …..
Galactose and fructose can also be converted in glucose in the liver

A

Glycerol/ adipose
Lactate/ anaerobic glycolysis
Amino Acids (Alanine)/ muscles

208
Q

Carboxylase ABC
A -…..
B- …..
C-……

A

Atp (needs energy)/ needs Biotin/ CO2 binds to biotin to be added

209
Q

Carboxylase ABC
A -…..
B- …..
C-……

A

Atp (needs energy)/ needs Biotin/ CO2 binds to biotin to be added

210
Q

In gluconeogenesis, Alanine is converted to Pyruvate in the …., using the enzyme ….. and vitamin …..

A

Liver/ Alanine aminotransferase (ALT)/ B6

211
Q

In gluconeogenesis, Lactate is converted to pyruvate using the enzyme ……

A

Lactate dehydrogenase

212
Q

In gluconeogenesis, pyruvate goes inside the mitochondria, but the acetyl-Coa formed from fatty acids (starvation) inhibits the enzyme ….., and stimulates the enzyme …….

A

Pyruvate dehydrogenase/ Pyruvate carboxylase

213
Q

In gluconeogenesis, the pyruvate is converted into ……, by the enzyme ……. Then, the …… goes back to the cytoplasm using the …..

A

OAA/ Pyruvate carboxylase/ OAA/ malate shuttle

214
Q

In gluconeogenesis, when OAA is in the cytoplasm, it’s converted to …. by the enzyme …..

A

PEP/ PEP carboxykinase

215
Q

In gluconeogenesis, the last two steps is responsible to …… the phosphates added in glycolysis, using the enzymes ……. and …….

A

Remove/ fructose 1,6 bisphosphatase/ glucose - 6 phosphatase

216
Q

In gluconeogenesis, glycerol is converted to …… , using the enzyme glycerol 3-phosphate dehydrogenase

A

DHAP

217
Q

Pyruvate carboxylase is a mitochondrial enzyme that is activated by …., from beta-oxidation. The product is …./ that can leave via …..

A

Acetyl CoA/ OAA/ malate shuttle

218
Q

In gluconeogenesis, the enzyme …… converts OAA to PEP in the cytoplasm , and it’s stimulated by …… and …..

A

PEP carboxykinase/ glucagon / cortisol

219
Q

Alcoholics are very susceptible to hypoglycaemia because of …. and …….

A

Poor nutrition/ high NADH formed by alcohol metabolism interferes with gluconeogenesis

220
Q

High NADH in alcohol metabolism favors the formation of:
1-……., from ……
2-……., from ……
3-……., from ……

A

Lactate/ pyruvate
Glycerol / DHAP
Malate / OAA in the cytoplasm

221
Q

Alcohol is converted into ….., by the enzyme….., in the ……

A

Acetaldehyde/ alcohol dehydrogenase/ cytoplasm

222
Q

Acetaldehyde is converted into ……., by the enzyme ……, in the …….

A

Acetate (acetyl CoA) / acetaldehyde dehydrogenase/ mitochondria

223
Q

Fomepizole is a long inhibitor of ……., preventing alcohol metabolism

A

Alcohol dehydrogenase

224
Q

Disulfiram inhibits the enzyme ….., increasing the concentration of acetaldehyde (hangover)

A

Acetaldehyde dehydrogenase

225
Q

Alcohol is converted into ….., by the enzyme….., in the ……

A

Acetaldehyde/ alcohol dehydrogenase/ cytoplasm

226
Q

Acetaldehyde is converted into ……., by the enzyme ……, in the …….

A

Acetate (acetyl CoA) / acetaldehyde dehydrogenase/ mitochondria

227
Q

Fomepizole is a long inhibitor of ……., preventing alcohol metabolism

A

Alcohol dehydrogenase

228
Q

Disulfiram inhibits the enzyme ….., increasing the concentration of acetaldehyde (hangover)

A

Acetaldehyde dehydrogenase

229
Q

Succinyl CoA is produced during the ….. and through ……

A

TCA cycle / VOMIT

230
Q

Alcohol is converted into ….., by the enzyme….., in the ……

A

Acetaldehyde/ alcohol dehydrogenase/ cytoplasm

231
Q

Acetaldehyde is converted into ……., by the enzyme ……, in the …….

A

Acetate (acetyl CoA) / acetaldehyde dehydrogenase/ mitochondria

232
Q

Fomepizole is a long inhibitor of ……., preventing alcohol metabolism

A

Alcohol dehydrogenase

233
Q

Disulfiram inhibits the enzyme ….., increasing the concentration of acetaldehyde (hangover)

A

Acetaldehyde dehydrogenase

234
Q

In gluconeogenesis, an obligate activator of the process is ……

A

Acetyl- CoA

235
Q

The two most common genetic cause of hemolitic anemia is
1- ….
2-…..

A

Glucose 6 Phosphate Dehydrogenase deficiency /

Pyruvate kinase deficiency

236
Q

In the G6PD deficiency, the hemolytic anemia is associated with ….., while in the pyruvate Kinase deficiency, the hemolytic anemia is associated with increased …..

A

Heinz bodies/ 2,3BPG (biophosphoglicerade)

237
Q

The absorbed fat bus is …..

A

Chylomicron

238
Q

Hexose monophosphate shunt, also called…… occurs in the …. of all cells, and has two major functions: ……. and …….

A

Pentose phosphate pathway/ cytoplasm/ produce NADPH/ produce ribose 5 phosphate for nucleotide synthesis

239
Q

Glucose 6 phosphate dehydrogenase is induced by ……, inhibited by ….., and activated by …..

A

Insulin/ NADPH/ NADP

240
Q

In the HMP shunt, ……. is responsible to do the shunt between ribose 5P and glycolysis metabolites

A

Transketolase

241
Q

In the liver, the G6PDehydrogenase makes …… to synthesise …., ….. and ……

A

NADPH/ fatty acid/ cholesterol/ nucleotides

242
Q

In the neutrophil, G6PD is responsible to make …. to activate the enzyme……, that is responsible to ….. bacteria

A

NADPH/NADPH oxidase/ kill

243
Q

In the erythrocytes, G6PD makes ….., that recycle ….., important to stop ……. When there’s a problem and ROS acumulate, it leads to ….. and ……

A

NADPH/ resuced glutathione/ ROS/ hemolytic anemia/ heinz bodies

244
Q

G6PD deficiency cause ……, …… and ……

A

Immune supression/ heinz bodies/ hemolytic anemia

245
Q

In patients with G6PD deficiency, the acute episodic hemolysis can be due to ……, …….. and …….

A

Fava beans ingestion/ drugs/ infection

246
Q

…….. and ……. are two essential fatty acids important in membrane phospholipids

A

Linolenic acid / linoleic acid

247
Q

In the fatty acid biosynthesis, malic enzyme is an additional source of ….. in the ……

A

NADPH/liver

248
Q

Acetyl CoA is transformed into ….. by the enzyme acetyl coa carboxylase

A

Malonyl CoA

249
Q

Acetyl CoA carboxylase is the rate-limiting enzyme of fatty acid biosynthesis thats is acrivated by ……. and …….

A

Insulin / citrate

250
Q

The VLDL is responsible for transport of triglycerides in fat ……, while Chylomicron is responsible for transport of triglycerides in fat ……

A

Synthesis/ digestion,absorption

251
Q

……. is the enzyme in the intestine that converts cholesterol to cholesterol esters for easier ….

A

ACAT/ storage

252
Q

Chylomicrons transport dietary …. and …… from ……. to tissues

A

Triglycerides/ cholesterol/intestine

253
Q

Apo B48 is ……. by the intestine with chylomicron.
Apo CII activates ……..
Apo E1 makes the ….. of …… by the liver

A

Secreted/
Lipoprotein Lipase/
Uptake/ remnants

254
Q

VLDL transport synthesised ….. from ……. to tissues

A

Triglycerides/ liver

255
Q

Apo B100 is ……. by the with VLDL.

A

Secreted/ liver

256
Q

LDL delivers ….. into cells via LDL receptor or …… receptor

A

Cholesterol / apoB 100

257
Q

CETP (cholesterol ester transfer protein) gives a cholesterol ester to ……, transforming it into …..

A

IDL/ LDL

258
Q

Chylomicrons and VLDL are primarily made of ……. particles

A

Triglyceride

259
Q

Lipoprotein Lipase hydrolyzes the …… from triglycerides, carried by …… and …….., and is activated by …..

A

Fatty Acid/ chylomicrons/ VLDL/ apo CII

260
Q

LDL and HDL are primarily …….. particles

A

Cholesterol

261
Q

Most of the cholesterol measured in the blood is associated with ……

A

LDL

262
Q

The normal role of LDL is to deliver …… to tissues for ….. When cell is ….. or …….

A

Cholesterol/ biosynthesis/ repairing membrane/ dividing

263
Q

Liver has multiple pathways for acquiring cholesterol, including …. synthesis, endocytosis of …., transfer of chesterol from …, endocytosis of …..

A

De novo/ LDL/ HDL/ chylomicron remnants

264
Q

Hugh cholesterol levels decrease gene expression of ……. and ……. (de novo synthesis)

A

LDL receptors (apo-100 receptors) / HMG- CoA reductase

265
Q

HDL is synthesized in the …. and ….. It contains ….. used for cholesterol recovery from fatty in the blood vessels.

A

Liver/ intestines/ apo-A1

266
Q

LCAT is an enzyme in the …… that is activated by …… on HDL. LCAT produces …….

A

Blood/ apoA-1/ cholesterol esters

267
Q

HDL cholesterols picked up in the periphery can be distributed to VLDL remnants (IDL) converting them to ….., using the enzyme…..

A

LDL/ cholesterol ester transfer protein (CETP)

268
Q

HDL cholesterols picked up in the periphery can also enter the cells through …. receptor

A

SR-B1

269
Q

Hyperlipidemia type I, also called …… can be caused by an genetic recessive lack of …. or ……, leading to increasing in …. and …..

A

Hypertriglyceridemia/ lipoprotein lipase/ apo CII / triglycerides/ chylomicron

270
Q

The symptoms of hypertriglyceridemia are (5 symptoms)

A

Xantomas/ fatty liver/ creamy serum/ pancreatitis/ abdominal pain after fatty meals

271
Q

Hyperlipidemia type II, also called …… can be caused by an genetic dominant lack of …., leading to increasing in ….

A

Hypercholesterolemia/ LDL receptor (apo B 100 receptor)/ LDL

272
Q

The hypercholesterolemia increase the risk of ….. and ….., the symptoms are (3 symptoms)

A

Artherosclerosis/coronary artery disease / xanthomas/ xanthelasmas/ corneal arcus

273
Q

Abetalipoproteinemia, also called ….., has low to zero serum ….. and ….. Serum tryglicerides and cholesterol are near …… The essential Fatty acids and vitamin A And E are not well absorbed

A

Hypolipidemia/ apoB 100/ apoB 48/ zero/

274
Q

The symptoms of Abetalipoproteinemia are (5 symptoms)

A
  • steatorrhea
  • ataxia
  • acanthocytes
  • loss of night vision
  • pigmentary degeneration in the retina
275
Q

Hyperlipidemia type III, is caused by a mutation in …., making ……leading to increasing in …., ….. and …..

A

Apo E/ ApoE 2/ tryglicerides/ cholesterol/ IDL

276
Q

Chilesterol is requires for (4 answers)

A

Membrane, steroids, vitamin D and bile acids synthesis

277
Q

In cholesterol synthesis, the rate limiting enzyme is ….., that is stimulated by …. and inhibited by ….., ……. and ……

A

HMG- CoA reductase/ insulin/ glucagon/ cholesterol/ statin drugs

278
Q

In the cholesterol synthesis, Farnesyl PPi is important for ……

A

Synthesis of CoQ (ETC)

279
Q

Statins reduce intracellular …..and increase …… of cholesterol (indirect increase in ……. on the membrane)

A

Synthesis of cholesterol/ absorption / LDL receptors

280
Q

Muscle weakness with statins are due to decrease in ……, that decrease…., decreasing ……, and decrease in cholesterol for …..

A

Farnesyl PPi/ coenzyme Q/ ETC activity/ membrane stability

281
Q

…… is a potent activator of acetyl-CoA carboxylase for fatty acid synthesis

A

Citrate

282
Q

HMG- CoA reductase produces ….. from …..

A

Mevalonate/ HMG- CoA

283
Q

In the RBC, NADH is responsible for ….., while NADPH is responsible for …..

A

MetHb reductase/ glutathione recycling

284
Q

In the RBC, NADH comes from ……

A

glycolysis

285
Q

Malonyl CoA is only in the cytoplasm when the liver is ……. fat

A

Synthesizing

286
Q

In postabsorbtive state, fall in insuline activates hormone-……. that hydrolyzes ….., yielding …. and ……

A

Hormone-sensitive lipase (HSL)/ triglycerides/ fatty acids/ glycerol

287
Q

Hormone-sensitive lipase (HSL) is released in the drop of ….., or increase of …… and …… However, it doesn’t respond to ……

A

Insulin/ epinephrine/ cortisol/ glucagon

288
Q

In high doses, Niacin works as antihyperlipidemic drug, inhibiting …… in adipose tissue

A

HSL/

289
Q

Long-chain fatty acids are transported into mitochondria by ….. to be oxidised

A

Carnitine transporter

290
Q

Carnitine acyltransferase-t (CAT 1) is inhibited by ….., from fatty acid synthesis

A

Malonyl - CoA

291
Q

Insulin indirectly inhibits B-oxidation by activating the enzyme ……, that increases….. Glucagon reverses the process

A

Acetyl CoA carboxylase/ malonyl CoA

292
Q

Each 4-step cycle of B-oxidation releases one ……, one ….. and one ……

A

Acetyl-CoA/ NADH/ FADH2

293
Q

The carnitine transport system is most important for allowing ……to enter the mitochondria

A

Long chain fatty acid

294
Q

Myopathic CAT/CPT Deficiency symptoms are (2 symptoms) and the common found in biopsy is …..

A
  • muscle pain and weakness in prolonged exercises
  • myoglobinuria
  • elevated muscle tryglicerides
295
Q

MCAD Deficiency symptoms are ……..(because of reduced gluconeogenesis), …….., ……., …….., …….. (because of increasing in peroxidation of fats), …….. (because of reduced urea cycle)

A
  • Fasting hypoglycaemia
  • No ketones bodies
  • C8/C10 fats in blood
  • vomiting, coma, death
  • dicarboxylic aciduria
  • hyperammonemia
296
Q

Fatty acids with odd carbon number are oxidised into ……, that is converted to …. in the TCA cycle

A

Propionyl-CoA/ Succinyl-CoA

297
Q

To form Succinyl-CoA, Propionyl-CoA uses the enzymes ….. and …… (requires Vitamin B12)

A

Propionyl-CoA carboxylase/ methylmalonyl-CoA mutase

298
Q

B12 Deficiency produces peripheral neuropathy due to aberrant fatty acid incorporation into the myelin sheets associated with inadequate …….. activity

A

methylmalonyl-CoA mutase

299
Q

In the fasting state, liver converts excess acetyl-CoA from B-oxidation of FA into ketone bodies (….. and ……)

A

Acetoacetate/ 3-hydroxybutyrate

300
Q

In ketogenolysis that happens is a non-hepatic cell, 3-hydroxybutyrate is converted to acetoacetate, that is converted back to acetyl-CoA by the enzyme ……

A

Thiophorase

301
Q

Alcoholics can also develop ketoacidosis, because chronic hypoglycaemia icreases ….. in the liver, but alcohol is converted to acetate in the liver, which is an alternative source of acetyl-CoA

A

ketone production

302
Q

Symptoms associated with ketoacidosis are

6 symptoms

A
  • polyuria, dehydration
  • thirst
  • CNS depression and coma
  • depletion of K
  • decreased plasma bicarbonate
  • breath with sweet or fruity odor (acetone)
303
Q

Sphingolipids are important constituents of cells membranes. It’s classified in three classes, according to the hydrophilic region: (3 classes)

A
  • sphingomyelin
  • Cerebrosides (glucose, galactose)
  • Gangliosides (GM-2)
304
Q

Tay- Sachs disease (Genetic Deficiency of Enzyme in Sphingolipid Catabolism):

  • Lysosomal enzyme missing: …..
  • Accumulation in Inclusion bodies: ….
  • Symptoms: (5)
A
  • Hexosaminidase A
  • Gangliosides GM2
  • cherry red spots in macula
  • death by 2
  • moro (startle) reflex
  • blindness
  • psychomotor retardation
305
Q

Gaucher disease (Genetic Deficiency of Enzyme in Sphingolipid Catabolism):

  • Lysosomal enzyme missing: …..
  • Accumulation in Inclusion bodies: ….
  • Symptoms: (5)
A
  • glucocerebrosidase
  • glucocerebroside
  • type I: hepatosplenomegaly
  • Erosion of bones/ fractures
  • pancytopenia/ thrombocytopenia
  • characteristic macrophages
  • crumpled paper inclusions
306
Q

Niemman-Pick disease (Genetic Deficiency of Enzyme in Sphingolipid Catabolism):

  • Lysosomal enzyme missing: …..
  • Accumulation in Inclusion bodies: ….
  • Symptoms: (5)
A
  • Sphingomyelinase
  • Sphingomyelin
  • Cherry red spots in macula
  • hepatosplenomegaly
  • microcephaly/ mental retardation
  • early death
  • foamy macrophages with zebra bodies
307
Q

Fabry disease (Genetic Deficiency of Enzyme in Sphingolipid Catabolism):

  • Lysosomal enzyme missing: …..
  • Accumulation in Inclusion bodies: ….
  • Symptoms: (5)
A
  • alpha- galactosidase
  • ceramide trihexoside
  • X-linked recessive (male)
  • Angiokeratomas
  • Cloudiness of cornea
  • burning sensation of hands
  • enlargement of heart and kidney
308
Q

In I cell disease, Golgi lacks ….., so it cannot target any enzyme to lysosome, leading to accumulation of multiple types of……. in the lisosome

A

Phosphotransferase/ inclusion bodies

309
Q

In most tissues, NH3 is added to glutamamate by the enzyme …… to form ….

A

Glutamine synthetase/ glutamine

310
Q

In the liver, glutamine is catabolised by the enzyme ….., forming ….. and ….

A

Glutaminase/ glutamate/ NH3

311
Q

In the starving liver, muscle releases …… that reacts with alpha ketoglutarate, using the enzyme ALT, to form …….. and …… The formed AA ….. reactas with OAA and form ……… (goes to urea cycle) and alpha ketoglutarate

A

Alanine/ pyruvate/ glutamate/ glutamate/ aspartate

312
Q

In the muscle, transaminases move the amino groups from many different AA onto ….. A portion of this AA will be aminated becoming ….., while the other part will become ……

A

Glutamate/ glutamine / alanine

313
Q

In the liver, transaminases (AST e ALT) move the amino group from alanine into …… to enter the urea cycle

A

Aspartate

314
Q

The essential AA are:

A

Phenylalanine
Valine
Threonine

Tryptophan
Isoleucine
Methione

Histidine
Argenine (condiotionally)
Leucine
Lysine

315
Q

Urea is synthesised in the liver, first, using …. and …… by the enzyme ….., to form …… This reaction needs on obligate activation, which is …..

A

Ammonium / CO2/ carbamoyl synthetase I/ carbamoyl phosphate/ N-acetylglutamate

316
Q

In the urea cycle, after carbamoyl phosphate is made, it’s gonna get attached to Ornithine, by the enzyme ……, forming …..

A

Ornithine transcarbamoylase/ citruline

317
Q

In the urea cycle, the mitochondrial enzymes are …… and ……

A

Carbamoyl phosphate synthetase I/ ornithine transcarbamoylase

318
Q

Aspartate enters the urea cycle in the cell ….. and leaves the cycle as ….. If gluconeogenesis is active, ……. can be converted to …….

A

Cytoplasm/ fumarate/ fumarate/ glucose

319
Q

In the urea cycle, when citruline goes to the cytoplasm it’s converted into ….., by the enzyme …..

A

Arginosuccinate/ arginosuccinate synthetase

320
Q

A disease called Arginosuccinate synthetase Deficiency is an autossomal recessive disease, characterised by elevated ……

A

Citruline

321
Q

Genetic Deficiencies of the Urea Cycle founds are ……, ……. and …….

A

Hyperammonemia/ elevated blood glutamine/ decreased BUN

322
Q

Carbamoyl Phosphate Synthetase Deficiency is an ……… recessive disease, and has …….. aciduria

A

Autossomal/ no orotic

323
Q

Ornithine Transcarbamoylase Deficiency is an ……… recessive disease, and has …….. aciduria

A

X-linked/ orotic

324
Q

Phenylketonuria is characterised by (5 characteristics). The treatment is based on …… and ……

A
  • Elevated phenylketones
  • Mental retardation
  • Mousy/Musty skin/urine odor
  • Avoid Aspartame
  • Diet important during pregnancy
    Low phenylalanine intake/ elevated tyrosine intake
325
Q

Tyrosine can be converted to Melanine using the enzyme …… and ….. A Deficiency of this enzyme cause …..

A

Tyrosinase/ Cu/ albinism

326
Q

Tyrosine is converted to DOPA by the enzyme ……. and …… For Parkinson disease, to increase Dopamine we can give a medication called ……, that can cross the blood-brain barrier

A

Tyrosine hydroxylase / THB/ levodopa (DOPA)

327
Q

Tyrosine is converted to DOPA, that is converted to Dopamine and then Norepinephrine. Norepinephrine is converted to epinephrine using the enzyme…….. and the AA……, that will be transformed into ……

A

Methyltransferase/ methionine / homocysteine

328
Q

Homocysteine can be converted back to methionine trough Methionine Recycling that uses the enzyme …… and the vitamins ….. and …..

A

Homocysteine methyltransferase / B12/ B9

329
Q

Besides being recycled to Methionine, Homocysteine can also be converted to ……., by the enzyme …… A defect on this enzyme cause ….. That is characterised by (7), and can be treated using….

A 
Cystathionine/ cystathionine synthase/ homocystinuria classical
- elevated homocysteine
- atherosclerosis 
- deep vein thrombosis 
- stroke
- Joint contractures
- Marfan like habitus
- mental retardation
B6
330
Q

Valine, Leucine and Isoleucine are branched chain AA, because they are metabolised by the enzyme …… A Deficiency on this enzyme cause …. That is characterised by (5). The treatment is …..

A 
Branched chain ketoacid dehydrogenase/ mapple syrupe urine disease/ 
- mapple syrup urine odor
- mental retardation
- ketosis
- coma, death
- abnormal muscle tone
Diet restriction
331
Q

On tyrosine waste pathway, it forms …… To break …… we need the enzyme …… A defect on this enzyme increases ….. leading to a disease named ….., characterised by (4)

A

Homogentistic acid/ homogentistic acid/ homogentistase oxdase / homogentistic acid/ Alkaptonuria

  • elevated homogentistic acid
  • dark urine
  • dark cartilage (ochronosis)
  • arthritis
332
Q

In biochemical reactions, when one carbon unit is needed, if it’s methyl, …… is the donnor, if a different group is required (methylene, methenyl..) …… is the donnor

A

S-adenosylmethionine (SAM)/tetrahydrofolate (THF)

333
Q

Tetrahydrofolate is formed from vitamin …. using the enzyme ….. It is important for …… and ….. synthesis. Methotrexate inhibits…… Folate deficiencies may be seen during ….. and ….

A

Folate/ dihydrofolate reductase (DHF reductase)/ purines/ thymidine/ DHF reductase/ pregnancy/ alcoholism

334
Q

Folate is needed for …… synthesis and …… recycling

A

DNA and RNA/ methionine

335
Q

The storage (reduced) form of THF is ……… This form is used by the enzyme ….. to make ….

A

N-methyl THF/ homocysteine methyl transferase/ methionine

336
Q

Folate Deficiency develops in 3-4 months and the risk factors are: (4)

A
  • pregnancy (neural tube defects in fetus)
  • alcoholism
  • gastric or terminal ilium resection
  • severe malnutrition
337
Q

Cobalamin Deficiency develops in years and the risk factors are: (9)

A
  • Severe malnutrition
  • Pernicious anemia
  • Gastric resection
  • Bacterial overgrowth of terminal ilium
  • Vegan
  • Aging
  • Chronic Pancreatitis
  • H pylori infection
  • Infection with Diphyllobotrium latum (parasite in raw fish)
338
Q

In the Heme Synthesis, the rate-limiting enzyme is ……, that needs …. to work, and produces …… This enzyme is inhibited by ….

A

Aminolevulinate synthase (ALA)/ B6/ Aminolevulinic acid/ Heme

339
Q

In the heme synthesis, porphobilinogen is metabolised by the enzime ……., also called ….., a deficiency on this enzyme cause ….., which the symptoms are autossomal ……., ……. onset, ……., ………….., increased ……., acute ……., ………., ………., ……..

A

Porphobilinogen deaminase/ hydroximethylbilane synthase/ acute intermittent porphyria/ dominant/ late/ episodic/ anxiety, confusion, paranoia/ porphobilinogen/ abdominal pain/ no photosensitivity (porphirin)/ port-wine (dark) urine(ogen)/ never give barbiturates

340
Q

In the heme synthesis, uroporphyrinogen III is metabolised by the enzime ……., a deficiency on this enzyme cause ….., which is the most …… porphyria, and the symptoms are (6)

A

Uroporphyrinogen decarboxylase/ porphyria cutanea tarda/

  • autossomal dominant
  • late onset
  • red-brown to deep-red urine
  • photosensitivity (inflammation, blister)
  • hyperpigmentation
  • exacerbated by alcohol
341
Q

In the heme synthesis, Lead (Pb) can inhibit two enzymes ……. and ……., causing the disease named …… In this disease we see an increase in …… and ……, because the enzymes won’t metabolise them

A

ALA dehydratase / ferrochelatase/ plumbism/ Aminolevulinic acid/ protoporphirin IX

342
Q

In heme synthesis, If ferrochelatase or Fe2+ are absent, there will be a non enzymatic insertion of ….. in protophorphyrin , which is easy to detect because it gets …..

A

Zn2+/ fluorescent

343
Q

Lead poisoning is a chronic disorder that happens more often in ….., that are exposed to …. and ….., causing symptoms (7), it causes ….., …… anemia. It can be treated using ……, …….. and ……

A 
Kids/ paint / plaster
- letargy
- headache
- nausea
- vomiting
- memory loss
- abdominal pain
- diarrhea or constipation
Mycrortic/ hypocromic
dimercaprol/ EDTA/ succimer
344
Q

B6 deficiency, iron deficiency and lead poisoning all can cause … Ringed sideroblasts are formed in ….. and ….

A

Microcytic Anemia/ B6 deficiency/ lead poisoning

345
Q

Ceruloplasmin (…. protein), also called …., oxidizes … to … for transport and storage. …… carries Fe3+ in the blood. …… binds excess Fe3+ to prevent escape of free Fe 3+ into the blood, where it is toxic

A

Cu/ Ferroxidase/ Fe2+/ Fe3+/ transferrin/ hemosiderin

346
Q

In the liver, bilirubin is converted to bilirubin diglucoronide by the enzyme…..

A

Glucuronyl transferase

347
Q

In Crigler Najjar syndromes, there’s a decrease in ….., leading to increase in …..

A

Glucuronyl transferase enzyme/ indirect bilirubin

348
Q

In Gilbert Syndrome there is a decrease in ….., leading to an increase of ….

A

Glucuronyl transferase affinity/ indirect bilirubin

349
Q

Conditions that increase indirect bilirubin are (5)

A
  • hemolysis
  • crigler najjar Syndrome
  • gilbert syndrome
  • low levels of conjugation enzyme in new borns
  • hepatic demage
350
Q

Conditions that increase direct bilirubin are (4)

A
  • hepatic demage
  • bile duct obstruction
  • rotor syndrome
  • dubin-johnson Syndrome
351
Q

Product formed by argininosuccinate lyase during urea cycle (2)

A

Arginine/ fumarate

352
Q

Substrate and energy source for synthesis of Aminolevulinic acid in heme pathway (2)

A

Glycine/ succinyl CoA

353
Q

The TCA cycle starts with acetyl Coa, that comes from ….. acetyl Coa is transformed into (8)

A

Pyruvate/

  • citrate
  • isocytrate
  • alpha ketoglutarate
  • succinyl CoA
  • succinate
  • fumarate
  • Malate
  • oxaloacetate
354
Q

Pyrimidine de novo synthesis happen in the …. using…., ….. and ….. The synthesis involves the enzyme ….

A

Cytoplasm/ aspartate/ CO2/ glutamine/ carbamoyl phosphate synthetase

355
Q

Pyrimidine de novo synthesis happen in the …. using…., ….. and ….. The synthesis involves the enzyme ….

A

Cytoplasm/ aspartate/ CO2/ glutamine/ carbamoyl phosphate synthetase

356
Q

Anything that messes with nucleotide synthesis can cause ….

A

Megaloblastic anemia

357
Q

Anything that messes with nucleotide synthesis can cause ….

A

Megaloblastic anemia

358
Q

Cells synthesize nucleotides in 2 ways: ….. synthesis and …. pathway

A

De novo/ salvage

359
Q

Pyrimidines are synthesised de novo from ……, …. and ….

A

Glutamine/ Aspartate/ CO2

360
Q

Cells synthesize nucleotides in 2 ways: ….. synthesis and …. pathway

A

De novo/ salvage

361
Q

In the de novo pyrimidines synthesis, Carbamoyl phosphate is converted to ….., which is converted to ….., by the enzyme …..

A

Orotic acid/ UMP (uridine)/ UMP synthase

362
Q

A decrease in the UMP synthase cause ….., where there’s an increase in ….. and …… anemia

A

UMP synthase/ orotic acid/ megaloblastic

363
Q

In the pyrimidines de novo synthesis, after UMP is made, thymidine synthesis starts with the enzyme …… This enzyme can be inhibited by ……

A

Ribonucleotide reductase/ hydroxyurea

364
Q

In the pyrimidines de novo synthesis, dUMP (dioxiuridine) is converted to dTMP (dioxithymidine) by the enzyme …., using vitamin ….. This enzyme can be inhibited by ….

A

Thymidylate synthase/ B9/ 5- fluoroutacil

365
Q

In the pyrimidines de novo synthesis, dUMP is converted to dTMP by the enzyme ….., using THF, producing…., that is converted back to THF by the enzyme….., that can be inhibited by ….., …… and …..

A

Thymidylate synthase/ DHF/ dihydrofolate reductase/ methotrexate/ trumethoprim/

366
Q

In the purine salvage pathway, AMP looses a .. and is converted to …., that is converted to …., by the enzyme…. A Deficiency on this enzyme cause ….. That is characterised by sever combined …..

A

P/ adenosine/ inosine/ adenosine deaminase/ Adenosine deaminase Deficiency / immunodeficiency

367
Q

In the purines salvage pathways, AMP and GMP are converted to ….. and …. It can be transformed into uric acid by the enzyme …… or go to the salvage pathway by the enzyme ……

A

Hypoxanthine / guanine/ xanthine oxidase/ HGPRT (HPRT)

368
Q

In the purines salvage pathway, a deficiency on the enzyme HGPRT causes ….., a …… recessive disease, characterised by (4)

A

Lesch-Nyhan syndrome/ X linked/

  • spastic cerebral palsy
  • self-mutilation
  • hyperuricemia and gout
  • extra nucleotide production
369
Q

In the purines salvage pathways, allopurinol and feboxustat inhibit the enzyme ….., inhibiting ….. production and preventing ….

A

Xanthine oxidase/ uric acid / tumor lysis Syndrome

370
Q

Allopurinol and 6-mercaptopurine nucleotide inhibit the ……. in the …… synthesis

A

PRPP amidotransferase enzyme / purine de novo

371
Q

HPRT is required for activation of the anticancer drug ……

A

6-mercaptopurine

372
Q

G6PD deficiency predisposes affected individuals to hemolysis in the presence of oxidizing agents such as the drugs ……, …. and …., and ingestion of …..

A

Primaquine (Anti malarials)/ sulfonamides/ dapsone/ fava beans

373
Q

Neonate with enlargement of spleen and chronic hemolysis is consistent with …….. deficiency. ……. deficiency doesn’t usually present splenomegaly, and hemolysis tends to be intermittent, when exposed to oxidative stress

A

Pyruvate kinase/ G6PD

374
Q

The anemia that is X linked is …..

A

G6PD deficiency

375
Q

The anemia that is autosomal recessive is …..

A

Pyruvate kinase Deficiency

376
Q

In …… deficiency, red cells are unable to produce sufficient ATP to maintain normal plasma membrane NaKATPase activity, causing swelling and lysis

A

Pyruvate Kinase/

377
Q

….. is the rate limiting enzyme of fatty acod biosynthesis. Its actuvated by ….. and …..

A

Acetyl CoA carboxylase/ insulin / citrate

378
Q

NH3+HCO3 are transformed into carbamoyl phosphate, using ….. and the enzyme …… The obligate activator of this enxyme is ……

A

2 ATP/ carbamoyl phosphate synthetase I/ N-acetylglutamate

379
Q

Ordinarily Careless Crappers Are Also Frivolous About Urination

A

Ornithine/ Carmabamoyl Phosphate/ Citruline/ Aspartate/ Arginosuccinate/ Fumarate/ Arginine/ Urea

380
Q

Pompe Disease is a glycogen storage disease, which the patient enzyme alpha 1,4 glucosidase is deficient, also called ….. On this disease we find glycogen like material in inclusion bodies, leading to cardiomegaly, muscle weakness and death by 2

A

Acid maltase

381
Q

During starvation, HCO3 levels ….., because it works as a buffer base for H+ produced by ketone bodies

A

Drop

382
Q

The hemorrhagic tendency in Vitamin K deficiency happens because glutammate residues on factors II,VII, IX and X must be converted to ….. for optimal activity

A

Gamma-carboxyglutamate residues

383
Q

Conversion of propionyl-CoA to methylmalonyl-CoA requires …..

A

Biotin

384
Q

Proline hydroxylation requires Vitamin C. A defect in collagen proline or lysine hydroxylation will affect ……, but will not prolong the ….

A

Partial Thromboplastin time/ PT

385
Q

G6PD deficiency is a …… recessive disease, while protein kinase is a ….. recessive disease

A

X-linked/ autossomal

386
Q

Fasting hypoglycemia and hypoketosis occuring together are strongly suggestive of a block in ……..

A

Fatty acid oxidation

387
Q

Dimercaprol(BAL), EDTA and succimer are used to treat ……….

A

Lead poisoning

388
Q

The substrate used for heme synthesis are …… and …….

A

Glycine/ succinyl-CoA

389
Q

Homocysteine synthesis cystathione using the enzyme ……. and vitamin ….. A defect on this enzyme cause ……, an autossomal recessive disorder characterized by (5)

A

Cystathione synthase/ B6/ homocystinuria/ deep vein thrombosis/ stroke/ atherosclerosis/ marfan like habitus/ mental retardation

390
Q

Lipoprotein lipase catalyzes the conversion of triglycerides in chylomicrons and VLDL to …… and …….

A

Free fatty acids/ glycerol

391
Q

…… is the main carbon source for gluconeogenesis in a dieting obese person

A

Glycerol

392
Q

Fatty acids that undergo B-oxidation produces acetyl-CoA, which does not make glucose. In the other hand, this process provide an important source of ATP and NADH to enable …… An exception for this statement is ……., that release one propionyl-CoA that is converted to …..

A

Gluconeogenesis/ odd-numbered fatty acids/ succinyl-CoA

393
Q

During diet by an obese, 80% of glucose comes from ……. During starvation, 80% of glucose comes from ……..

A

Glycerol/ AA degradation

394
Q

A condition caused by protein-energy malnutrition (adequate calories from carbohydrates but insufficient calories from protein) is named …

A

Kwashiorkor

395
Q

Lipoprotein Lipase (LPL) is located on The …. of adipose tissue for storage and other tissues with tryglicerides needs such as skeletal muscle, cardiac muscle, lacting breast

A

Vascular endothelium

396
Q

Norepinephrine to epinephrine by ……

A

Phenylethanolamine N-methyltransferase (PNMT)

397
Q

The essential fatty acids are ….. and …… They …… be synthesized by healthy adults but are ubiquitous in natural diets.

A

linoleic acid/ linolenic acid/ cannot

398
Q

Folic acid is produced by ……. from the precursor p-aminobenzoic acid. This production is inhibited by ….. antibiotics. Folic acid is also obtained from green leafy vegetables and …….

A

symbiotic bacteria/ sulfa/ cereal

399
Q

Molar pregnancy classically manifests with the triad of ….., ……., and …… Investigators hypothesize that the symptoms of …… may arise because of homology between the structure of hCG and thyroid-stimulating hormone (TSH). In such patients, the high levels of β-hCG presumably cross-react with TSH receptor sites. β-hCG, TSH, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) all share the same α-subunit but have different β-subunits.

A

hyperemesis/ vaginal bleeding/ hyperthyroidism/ hyperthyroidism

400
Q

……, also known as lecithin, is the dominant component of pulmonary surfactant. Pulmonary surfactant consists of phospholipids (85%), proteins (10%), and neutral lipids (5%). About 75% of the phospholipids in surfactant are composed of ……..

A

Phosphatidylcholine/ phosphatidylcholine

Biochemistry (1 decks)

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