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BIOCHEMISTRY Flashcards

1
Q

RLE of glycolysis

A

step 3) phosphofructokinase-1

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2
Q

enzymes of irreversible steps of glycolysis ‘thermodynamic barriers’

A

step 1) glucokinase / hexokinase
step 3) phosphofructokinase-1
step 9) pyruvate kinase

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3
Q

irreversible steps of glycolysis

A

step 1) glucose –> glucose-6-phosphate
step 3) fructose-6-phosphate –> fructose-1-6-bisphosphate
step 9) Phosphoenolpyruvate –> pyruvate

glucose - G6P
F6P - F16BP
PEP - pyruate

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4
Q

what step does fluride inhibit in glycolysis

A

step 8) 2-PG –> PEP
removes Mg2+ & causes irreversible inhibition of enzyme enolase

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5
Q

what does Arsenate inhibit in glycolysis

A

stage 6) glyceraldehyde-3-P –> 1-3-bisphosphoglycerate
competes with PO4 for binding site on 1-3-BPG, no ATP produced

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6
Q

what step of glycolysis uses NADH

A

step 5) glyceraldehyde-3-phosphate –> 1-3-bisphosphoglycerate
uses: 2 NAD+ –> 2 NADH

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7
Q

what steps of glycolysis use (cost) ATP?

A

ATP –> ADP
step 1
step 3

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8
Q

whats steps of glycolysis produce ATP?

A

ADP –> ATP
step 6) 1-3-bisphosphoglycerate –> 3-phosphoglycerate
step 9) PEP –> pyruvate

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9
Q

what upregulates glycolysis?

A

insulin
ADP
AMP
Fructose-2-6-BP
Fructose-1-6-BP (at step 9)

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10
Q

what downregulates glycolysis

A

ATP
citrate
glucagon
alanine (at step 9)
acetyl-COA (at atep 9)

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11
Q

what gluconeogenesis enzymes differ from glycolysis?

A

(from top of glycolysis flowchart)
step 1) Glucose-6-phosphate
step 3) fructose-1-6-bisphosphate 1

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12
Q

how much energy produced from glycolysis

A

2 ATP
2 NADH

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13
Q

how much energy is produced from gluconeogenesis

A

4 ATP
2 GTP
2 NADH

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14
Q

gluconeogenesis can also occur from oxaloacetate in the TCA cycle via what enzyme?

A

oxaloacetate (TCA) –> PEP (Gluconeogenesis)
enzyme: PEP carboxykinase

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15
Q

in gluconeogenesis what co-factor does the enzyme require to convert pyruvate –> oxaloacetate

A

B7 (Biotin)
with pyruvate carboxylase
(occurs in mitochondria)

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16
Q

what stages of TCA cycle require (5) co-factors

A

B1, B2, 3B, B5, lipoic acid

step 1) pyruvate –> acetyl-CoA
enzyme: pyruvate dehydrogenase

step 6) a-ketoglutarate –> succinyl-CoA
enzyme: a-ketoglutarate dehydrogenase

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17
Q

what step of gluconeogenesis uses GDP as phosphate donor

A

oxaloacetate –> PEP
(step 2)

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18
Q

Pyruvate can be converted to ( ) or ( ) during intense exercise or starvation states & using which enzymes

A

cori cycle: lactate
lactate dehydrogense (LDH)
cahill cycle: alanine:
alanine transaminase (ALT)

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19
Q

how much energey is produced by TCA cycle

A

2 cycles:
3 NADH (= 2.5 ATP)
1 FADH2 (= 1.5 ATP)
1 GTP per acetyl-CoA (= 1ATP)
2 Co2
….. 20 ATP

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20
Q

what is the RLE of TCA cycle

A

isocitrate dehydrogenase
isocitrate –> a-ketoglutarate
step 4: (from pyruvate)

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21
Q

what enzymes of TCA cycle use NADH

A

step 4) isocitrate dehydrogenase
isocitrate –> a-ketoglutarate
step 5) a-ketoglutarate dehydrogenase
a-ketoglutarate –>succinyl-CoA
step 9) malate dehydrogenase
malate –> oxaloacetate

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22
Q

what step uses FADH2 in TCA cycle

A

step 7) succinate dehydrogenase
succinate –> fumerate

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23
Q

what enzyme of TC cycle odes arsenite inhibit

A

step 1) pyruvate dehydrogenase
pyruvate –> acetyl-CoA

24
Q

what step of TCA uses GTP

A

step 6) succinate thiokinase
succinyl-CoA –> succinate

25
what are the regulatory enzymes in TCA cycle
step 2) citrate synthase step 4) isocitrate dehydrogenase (RLE) step 5) a-ketoglutarate dehydrogenase
26
newborn metabolic acidosis tachypnoea hypoglycaemia ketosis **hyperammonia** vomiting, dehydration, AMS
methylmalonic acidaemia (or propionic acidaemia) *'organic acidemia'* | propionic acidaemia - would have low methylmalonic acid ## Footnote accumulation of methylmalonate inhibits urea cycle --> hyperammonia * Urea cycle defects typically show no ketosis, while organic acidemias show ketosis + hyperammonemia, as in this case.*
27
sNRPs are _\_\_ at the _\_\_
**single base** substitutions at the **splice acceptor site**
28
transcription is the process where -? is made from -?
pre-mRNA DNA ## Footnote pre-RNA must undego post-transcriptional modification to create mature mRNA i.e. removal of interons (by SnRPs)
29
pre-RNA must undego _\_\_ to create mature mRNA
****post-transcriptional modification | i.e. removal of introns (by SnRPs)
30
mutation at** splice acceptor site** can result in
inclusion of interions exclusion of exons non-functional mRNA / protein
31
SRP (signal recognition particle) function
traffics polypeptide-ribosome complex from the **cytosol** to the **RER** ## Footnote occurs after transcription
32
location of SRP (signal recognition particle)
**cytosolic** ribonucleoprotein
33
organic chemical compound is found in **paint thinner**
methanol
34
toxic metabolite of **methanol** metabolism
formic acid ## Footnote **anion gap metaboic acidosis** compensatory respiratory alkalosis **retinal** oedema putaminal haemorrhage optic disc hyperaemia GIT distress neurologic depression
35
_\_\_-chain fatty acids don't require carnitine shuttle
medium
36
****long chain fatty acids require _\_\_ enzyme to **shuttle** them from cytoplasm into mitochondrial matrix
carnitine-acylcarnitine translocase | carnitine shuttle ## Footnote enzyme dysfunction LCFA nt shuttled accumulate in liver/muscles
37
AR childhood onset encephalopathy, vomiting, hypoketotic hypoglycemia hyperammonemia muscle weakness, skeletal myopathy cardiomyopathy, ventricular dysrhythmias | enzyme deficiency carninte shuttle
carnitine-acylcarnitine translocase deficiency | can't shuttle LCFA
38
symptoms of carnitine-acylcarnitine translocase deficiency triggered by
illness fasting ## Footnote Tx medium chain fatty acids low fat, high carb formula **carnitine** supplement
39
Lesch-Nyhan; defect in _salvage_ of
guanine hypoxanthine | defect in HGPRT ***decreased** levels* guanine, hypoxanthine ## Footnote ***increased*** levels xanthine, uric acid
40
folate has what affect on; **homocystine methylmalonic acid**
increased normal ## Footnote homocyteine --> methionine (folate & B12) methylmalonyl-CoA - succinyl-coA (B12)
41
folate deficiency common in (4)
malnutrition alcoholism high cell turn over - *leukaemia, sickle cell* anti-folate drugs
42
mutations in Kosak sequence impair | eukaryotes
translation of proteins | AUG methionine start codon ## Footnote i.e. seen in B-thalassemia (point mutation affecting start codon)
43
what location is the cause of OTC deficiency ## Footnote ornithine transcarbamylase (OTC) deficiency
C
44
male newborn lethargy, poor feeding, vomiting 4 increased ammonia and orotic acid.
OTC deficiency | ornithine transcarbamylase (OTC) deficiency
45
what is increased in ornithine transcarbamylase (OTC) deficiency
orotic acid (from accumulation carbamoyl phosphate) | decreased citrulline ## Footnote hyperammonia
46
altered consciousness from DKA causing dehydration can alter consciousness via | glucose
osmotic diuresis | glucose in the urine draws water with it ## Footnote hyperosmolar hyperglycemic state (HHS) diabetic ketoacidosis (DKA)
47
Urea cycle defects typically show no _\_\_ while organic acidemias show _\_\_ + _\_\_
ketosis ketosis + hyperammonemia
48
generalized weakness numbness and tingling UL/LL difficulty walking ataxic gait decreased DTRs haemolytic anaemia | vitamin deficiency
vitamin E | peripheral neuropathy ## Footnote antioxidant protects erythrocytes from free radicals can be seen in **cystic fibrosis **-> problem absorbing fat-sol vitamins DEAK - pancreatic insufficiency CF + vitamins -> think pancreas
49
peripheral neuropathy dermatitis sideroblastic anaemia glossitis seizures
vitamin B6 (pyridoxine) | seizures espeicially if isoniazid use setting ## Footnote deficiency limits sythesis histamine, Hb and neurotransmiters
50
what **enzyme** does both liver and kidney possess to permit release of free glucose into the serum
**glucose-6-phosphat_ase_** | liveer - glucogenolysis & gluconeogenesis kidney - gluconeogenesis ## Footnote used during strenuous exercise G-6-P hydrolyses glucose-6-phosphate to create free glucose molecules
51
*endocytosis* is affected by mutation in the _\_\_ domain of LDL receptor
cytoplasmic **signalling** for **endocytosis** occurs via **cytoplasmic domain** ## Footnote extracellular domain mutation would affect LDL particles binding to LDL receptor
52
enzyme defects (2) causing **homocystinuria**
cystathionine b-synthase (↑ methionine) methione synthase (↓ methionine) | look for difference in methionine concentration ## Footnote homocysteine → cystathionine (requires vitamin B6) homocysteine → methionine (requires vitamin B12)
53
in apoptosis what activatescaspase enzymes
cytochrome c | once in cytoplasm releases caspases ## Footnote Bax and Bak interact with outer cellmembrane --> induce permeability -> release of cytochrom c into cytoplasms cause: **cell shrinkage nuclear pyknosis (condensed chromatin) karyorrhexis (fragmentation nucleus) blebbing membrane** apoptotic bodies
54
list 5 things seen in apoptotic cell
**cell shrinkage nuclear pyknosis (condensed chromatin) karyorrhexis (fragmentation nucleus) blebbing membrane** **apoptotic bodies** | no inflammation (unlike necrosis)
55
TATA lies upstreasm of transcription start site and funcitons as a binding site for
RNA polymerase ## Footnote mutation in TATA sequence or promoter = decreased gene trasnscription (as inability of RNA polymerase to bind to promoter)
56
non-coding regulatory sequence that governs transcription
TATA box | **regulatory proteins **i.e. TP53 also bind to theis region ## Footnote DNA also contains non-coding sequenceinf (enhancer, silencer regions) that augment or inhibit transcription of regulated genes
57
how is gout caused is it related to any specific inborn errors of metabolism or organ dysfunction
purine ric diet i.e. red meat/seafood, males, 4-7th decade (uric acid accumulation) lifestyle factors - no inborn errors/organ dysf

BSIC (27 decks)

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