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Pass Program > Chapter 6: Anabolic Pathways > Flashcards

Chapter 6: Anabolic Pathways Flashcards

1
Q

Do anabolic pathways happen in fed state or starvation state?

A

fed state (anabolic is building)

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2
Q

lipids, proteins, glucose, ketones, glycogen, glucose: in what order are these broken down and in what order are they built back up

A

broken down: glucose, glycogen, protein, lipids, ketones
built up: same order as above

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3
Q

What hormone allows us to take in glucose?

A

insulin

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4
Q

What are the second messengers for insulin?

A

tyrosine kinase, parasympathetic cGMP

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5
Q

What anabolic pathway does glucose activate and which catabolic pathway does glucose inhibit?

A

glucose activates glycogen synthesis and inhibits gluconeogenesis

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6
Q

5 areas of glycogenesis

A

liver, skeletal muscle, adrenal cortex, intestinal wall and heart

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7
Q

What are the only 2 organs that can use glycogen for glucose and put it into bloodstream?

A

liver and adrenal cortex

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8
Q

What drug inhibits gluconeogenesis?

A

metformin

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9
Q

Which diabetes drug blocks the voltage sensitve potassium channels and promotes insulin release?

A

sulfonylureas

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10
Q

SE of sulfonylureas

A

hypoglycemia, sulfa drug reactions, SIADH (Chlorpropamide)

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11
Q

Which DM2 drug blocks postprandial absorption of glucose?

A

alpha glucosidae inhibitors: acarbose, miglitol

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12
Q

SE of alpha glucosidase inhibitors

A

abdominal pain, gas, bloating, nausea

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13
Q

If a person is taking metformin, what must you do if he/she needs a contrast CT?

A

Stop metformin for a few days, then perform CT; if acute, stop metformin, give IV fluids and add NAC to protect kidneys.

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14
Q

Name a few thiazolidinediones for DM2

A

pioglitazone, rosiglitazone

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15
Q

Name a few incretin mimetics. What do they do?

A

exenatide, semaglutide: mimic incretins that are secreted by intestinal wall in response to food; potentiates insulin release, inhibits glucagon release, inhibit appetite and food intake (Ozempic)

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16
Q

DPPP4 inhibitors

A

inhibits degradatoin of GLP-1; more insulin release, inhibit glucagon release

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17
Q

two short acting insulin

A

regular and lispro

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18
Q

two medium length insulins

A

NPH and lente

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19
Q

two long acting insulin analogs

A

ultralente; glargine

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20
Q

What kind of bonds are involved in glycogen chain?

A

alpha 1,4 bonds

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21
Q

After 8 to 10 bonds on glycogen chain, what kind of bond is needed to branch the chain?

A

alpha 1,6 bond

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22
Q

Which glycogen storage disease has only straight chains and no branching enzyme?

A

Anderson’s Disease

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23
Q

What pathway makes ribose 5 phosphate used in DNA and RNA synthesis and NADPH as a byproduct?

A

pentose pathway (HMP shunt)

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24
Q

What are the uses of NADPH?

A

DNA synthesis, fatty acid synthesis, RBC repair (glutathione)

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25
Q

What happens in G6PD deficiency?

A

cannot repair RBC; cannot protect against sulfur reactions

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26
Q

List the X-linked recessive enzyme deficiencies

A

GOLF PAATCHS
G6PD
OTC
Lesch-Nyhan (HGPRT)
Fabry’s (alpha-galactosidase)
PRPP Synthetase
Adenosine Deaminase
Adrenoleukodystrophy (CAT-1)
Tyrosine Kinase
CGD (NADPH-oxidase)
Hunter’s (iduronidase)

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27
Q

In alcoholics, what do you add to IV before administering glucose?

A

Thiamine! otherwise brain cells will swell and burst causing Wernicke’s encephalopathy and Wernicke’s aphasia

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28
Q

With GGT what is the product of this: carbon+ glutamic acid yields _______________

A

AA + alpha ketoglutarate

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29
Q

With AST what is the product of this: oxaloacetate + AA yields ___________

A

aspartate + carbons

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30
Q

With ALT what is the product of this: pyruvate + AA yields __________

A

alanine + carbons

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31
Q

What destroys all membranes?

A

alcohol

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32
Q

Why in alcoholics AST: ALT is 2:1

A

because the mitochondrial membrane is destroyed, both AST and GGT will leak out as well as one AST and one ALT from cell membrane, making AST:ALT 2:1 and GGT goes up

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33
Q

What does the COX pathway synthesize?

A

prostaglandins

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34
Q

What does the LOX pathway synthesize?

A

leukotreines

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35
Q

If you block the COX pathway which way will the pathway go?

A

to LOX and vice versa

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36
Q

5 things steroids do

A

IKISS
Inhibit Phospholipase A
Kills T cells and eosinophils
Inhibits macrophage migration
Stabilize mast cells
Stabilize endothelium

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37
Q

What does prostaglandin A2 do?

A

promotes platelet aggregation

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38
Q

What does prostaglandin E1 do?

A

vasodilator, keeps PDA open; Misoprostol: treatment of aspirin induced ulcers and abortifacient
Alprostadil; keeps PDA open

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39
Q

What does Prostaglandin E2 do?

A

Dinoprostone: labor induction, dilates cervix

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40
Q

What does Prostaglandin I2 do?

A

dilates pulmonary vessels; inhibits platelet aggregation

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41
Q

What does Prostaglandin F2 do?

A

responsible for dysmenorrhea (period cramps); separates placenta after fetal delivery, abundant in semen Specific PGF-2s Carboprost -abortifacient Latanoprost; –glaucoma med

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42
Q

Where is COX 1 found?

A

GI tract

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43
Q

Where is COX 1 and 2 found?

A

joints

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44
Q

Where is COX 2 found?

A

vascular endothelium

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45
Q

What are SRS-A (slow reacting substance of anaphylaxis)

A

leukotreines

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46
Q

Which cells make leukotreines?

A

mast

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47
Q

Which leukotreines are involved in anaphylaxis (SRS-A)?

A

LTC4, LTD4, LTE4

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48
Q

What breaks down slow reacting substance of anaphylaxis SRS-A?

A

aryl sulfatase

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49
Q

What is aryl sulfatase deficiency?

A

metachromatic dystrophy: ataxia, visual disturbance (bumping into furniture), learning impaired

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50
Q

What leukotriene along with IL-8 is a strong chemoattractant for neutrophils?

A

LTB-4

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51
Q

What is a clue for aspirin-sensitive asthma?

A

bronchoconstriction upon taking aspirin and nasal polyps

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52
Q

What is cinchonism?

A

thrombocytopenia, hearing loss (CN8); tinnitus

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53
Q

What medicine is classic for cinchonism?

A

aspirin

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54
Q

At the beginning of aspirin toxicity (within 20 min) what is the RR, pCO2, HCO3- and pH?

A

RR up; pCO2 down, HCO3-normal; pH high=respiratory alkalosis

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55
Q

between 30 - 60 minutes of aspirin toxicity?

A

RR up; pCO2 low, HCO3- Low, pH normal; respiratory alkalosis and metabolic acidosis

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56
Q

after 60 minutes GABA increases what is the RR, pCO2, HCO3-, pH

A

RR down; pCO2 up; HCO3-down; pH low mixed acidosis (anion gap acidosis)

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57
Q

Which medicine can close PDA?

A

IndomethiCin (C for close)

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58
Q

Which NSAID is topical?

A

Diclofenac, Ketoprofen

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59
Q

What is the main oral steroid?

A

prednisone

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60
Q

What is the main IV steroid?

A

methylprednisone

61
Q

What is the DOC steroid to produce surfactant in premature delivery?

A

Dexamethasone

62
Q

Best drug to take place of cortisol

A

hydrocortisol

63
Q

best drug to take place of aldosterone

A

fludrocortisone

64
Q

Which steroid is used to treat endometriosis?

A

Danazol (androgenic) SE: hirsutism, weight gain, insulin resistance

65
Q

What is a 16 carbon fatty acid attached to C3 of G3P?

A

triglyceride

66
Q

What is cellular marker for apoptosis?

A

phosphatidylserine

67
Q

If an OH group is attached to C3 instead of phospate, what is it?

A

DAG used in IP3-DAG second messenger system

68
Q

Which hypothalamic hormone does not use IP3-DAG system?

A

CRH

69
Q

What are lacteals?

A

lymphatic channels for lipid absorption

70
Q

Short, medium, long chain fattly acids, which first go into lacteals?

A

short and long

71
Q

How can medium chain FA be absorbed?

A

attached to albumin, and can be absorbed even by IBD pts.

72
Q

Which medicine blocks lateals and doesn’t allow fat absorption?

A

Ezetimibe

73
Q

What needs CII from HDL to transport long chain fatty acids to adipose?

A

VLDL

74
Q

Which apolipoprotein is missing in apolipoproteinemia?

A

Apo B48

75
Q

What is the deficiency in Type 1 dyslipidemia?

A

lipoprotein lipase deficiency

76
Q

What is the deficiency in Type 5 dyslipidemia?

A

lipoprotein and CII deficiency

77
Q

What is the deficiency in Gaucher Disease?

A

Glucocerbrosidase; macrophages look like crinkled paper

78
Q

What is the deficiency in Fabry’s disease?

A

alpha-galactosidase (X-linked recessive); cataracts; early renal failure

79
Q

What is the deficiency in Krabbe’s?

A

beta-galactocerbrosidase causing globoid bodies (macrophages swollen with sugar)

80
Q

What is the deficiency in Tay Sach’s?

A

Hexosaminidase A; cherry red macula, fine for first few years then regressive development

81
Q

What is the deficiency in Sandhoff’s?

A

Hexosaminidase A and B; cherry red macula, more severe than Tay-Sach’s

82
Q

What is the deficiency in Niemann-Pick?

A

shingomyelinase, cherry red macula, hepatosplenomegaly sets it apart from Tay Sach’s or Sandhoff’s

83
Q

What is the deficiency in Matachromatic Leukodystrophy?

A

arylsulfatase deficiency; “childhood MS”; demyelinated plaques on LP; MRI shows demyelination

84
Q

What is the deficiency in Hurler’s?

A

alpha L iduronidase; Gargolye features; cataracts

85
Q

What is the deficiency in Hunter’s?

A

Iduronidase sulfatase; XL recessive, no cataracts

86
Q

What is the deficiency in Metachromatic Leukodystrophy?

A

arylsulfatase deficiency; “childhood MS”; demyelinated plaques on LP

87
Q

What enzyme do statins work on?

A

HMG-COA reductase

88
Q

What is the remnant of VLDL and IDL?

A

LDL

89
Q

What lipoprotein does LDL use to deposit cholesterol into tissues?

A

B-100

90
Q

3 signs of common bile duct gallstone

A

pancreatitis, ALP up, WBC up and fever

91
Q

What is the rate limiting enzyme for Urea cycle?

A

carbamoyl phosphate sythetase 1 (CPS-1)

92
Q

If there is an enzyme deficiency early in the Urea cycle, what will you see in urine or plasma?

A

High ammonia

93
Q

If there is an enzyme deficiency late in the pathway, what will you see?

A

serum pH is high (alkalotic); pyrimidines in the urine

94
Q

MCC of liver failure?

A

NAFLD (alcohol #2)

95
Q

Tx for liver failure

A

low protein diet (less than 2g/day); lactulose to flush out GI, NO fat-soluble drugs, P450 dependent drugs, benzos, barbs, GABA enhancers, alcohol

96
Q

Glutamate cannot enter urea cycle, add another amine to it and turn it into glutamine to excrete in kidney, but kidney can only excrete 10%, eventually GABA rises, this is called ______

A

Hepatorenal Syndrome

97
Q

If you want to add 1 sugar to anything what do you use?

A

UDP

98
Q

If you want to add phospholipids what do you use?

A

CDP

99
Q

What is the methyl donator in whole body except for nucleotides?

A

SAM

100
Q

What is the methyl donor in nucleotides?

A

THF

101
Q

3 ways to distinguish B12 from B9 deficiency:

A

B12 takes a longer time to deplete (years); B12 deficiency is associated with neuropathy; up methylmalonic acid in urine

102
Q

If you want to silence DNA what enzyme can you use?

A

methylation (tightens DNA–methylation down with aging, more Gs and Cs)

103
Q

If you want to loosen up DNA?

A

acetylation of histone (add A+T)

104
Q

What happens to DNA upon UVB light?

A

form Thymidine dimers

105
Q

What enzyme can snip out thymidine dimers?

A

UV endonuclease

106
Q

What disease is associated with partial deficiency of UV light endonucleases?

A

Ecthyma or Ichthyosis

107
Q

What disease is associated with complete deficiency of UV light endonucleases?

A

Xeroderma Pigmentosa

108
Q

What disease is associated with too many DNA breaks from free radicals?

A

Ataxia Telangiectasia (spider veins, IgA def. ; malabsorption of GI

109
Q

What is another name for Hereditary Non-polyposis colon cancer?

A

Lynch

110
Q

If PRPP is high which path will it take?

A

De Novo, higher Km (needs more energy)

111
Q

If PRPP is low which path will it take?

A

salvage, lower Km (needs less energy)

112
Q

What is the rate limiting enzyme of Purine Pathway?

A

PRPP synthetase+

113
Q

What three things are needed for membrane movement?

A

ATP,Ca, microtubules

114
Q

Tx for acute gout?

A

indomethacin

115
Q

best Tx for gout? and MOA

A

colchicine, blocks microtubules and interferes with cellular division and inflammatory cell mobility

116
Q

best tx for gout if pt has renal failure

A

steroids (injected into affected joints) because indomethacin and colchicine are water soluble and toxic to kidney

117
Q

best tx for chronic/recurring gout

A

allopurinol or Febuxostat (MOA: blocks xanthine oxidase)/ Probenicid (promotes uric acid excretion)

118
Q

tx for chemotherapy pts with hyperuricemia?

A

fluids and allopurinol

119
Q

What is the enzyme deficiency of Lesch-Nyhan Syndrome?

A

HGPRT deficiency; severe gout with self-mutilation

120
Q

What’s the difference between uracil and thymidine?

A

thymidine contains a methyl group (from THF)

121
Q

What does 5 Flourouracil do?

A

inhibits thymidylate synthetase (break down pyrimidine synthesis–CA drug)

122
Q

What disease is caused by adenosine deaminase deficiency?

A

SCID (2/3 XL; 1/3 AR IL2, !L7 defect)

123
Q

Tx for SCID

A

bone marrow transplant

124
Q

explanation of SCID

A

adenosine deaminase deficiency causes dATP levels to increase–ribonucleotide reductase activity decreases–DNA syntehsis decreases–rapidly dividing cells affected most (deplete bone marrow)

125
Q

Any cancer ages 0-20 are usually caused by repressor genes or enhancer genes?

A

repressor; K-ALLA (ALL), Rb

126
Q

What enhancer mutation can cause follicular lymphoma or Burkitt’s lymphoma?

A

BCL2

127
Q

What enhancer mutation can cause GI or Bone marrow cancers?

A

KRAS

128
Q

What enhancer mutation can cause melanoma?

A

BRAF

129
Q

Which ribosomes will make the proteins that stay in the cytoplasm?

A

free floating ribosomes

130
Q

Which ribosomes make the proteins that will be secreted out of the cell?

A

fixed ribosomes (fixed to RER)

131
Q

What is messenger RNA job?

A

transcribe DNA to mRNA, 3’ end poly A tail, 5’ end guanosine cap with methyl group

132
Q

Which proteins are responsible for splicing out introns and bringing exons together posttranscriptionally?

A

SNRPs

133
Q

Which RNA is used in translation?

A

transfer RNA

134
Q

Which disease has anti-RNP?

A

mixed connective tissue (antibody against SNRPs)

135
Q

Which enzyme replicates rRNA?

A

RNA polymerase I

136
Q

Which enzyme helps replicate mRNA

A

RNA polymerase II

137
Q

Which enzyme helps replicate tRNA and SNRPs?

A

RNA polymerase III

138
Q

What is the start codon for tRNA?

A

AUG

139
Q

What are the stop codons for tRNA?

A

UAA, UAG, UGA (u are away, u are gone, u go away)

140
Q

Where does mRNA bind initiation factors IF-1, IF-2, IF-3 in prokaryotes? AGGAGG

A

Shine-Dalgarno sequence

141
Q

Which antibiotic blocks initiation factors in prokaryotes?

A

aminoglycosides

142
Q

Which two diseases are associated with EF-2 elongation?

A

diptheria, pseudomonas

143
Q

Which antibiotics block translocase?

A

macrolides

144
Q

Which kind of mutations often happen in diseases from birth/ early childhood?

A

frameshift

145
Q

Which mutations are a change in one base at one point and occurs with a DNA base from same family (purine-purine) (pyrimadine-pyrimadine)?

A

transition mutation

146
Q

Which mutations are a change in one base at one point but occurs from different DNA family? (purine –pyrimadine)

A

transversion mutation

147
Q

Which mutation there is a change in one base but still codes for same amino acid and is asymptomatic?

A

silent mutation (HbC sub lysine for glutamic acid at position 6 of beta chain, asymptomatic)

148
Q

What mutation changes in one base and now codes for different amino acid, i.e. in sickle cell)?

A

missense mutation (sickle cell, valine for glutamate)

149
Q

Which mutation there is a change in one base and it becomes a stop codon?

A

nonsense mutation (occurs early in life)

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