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Tung Tung Tung Tung Sahur > Metab > Flashcards

Metab Flashcards

1
Q

What are the key steps of glycolysis

A

Glucose -> G6P (Hexokinase/Glucokinase)
F6P -> F-1,6-BP (PFK1)
Phosphoenolpyruvate -> Pyruvate (PK)

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2
Q

Describe how F-2,6-BP is regulated

A

Low energy state
- Increase glucagon => phosphorylation into active FBP2 => increase F-2,6-BP -> F6P => decrease PK activity and glycolysis

High energy state
- Increase insulin => dephosphorylation into active PFK2 => increase F6P -> F-2,6-BP => increase PK activity and glycolysis

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3
Q

What are the pathways that pyruvate can take

A

Pyuruvate -> Acetyl CoA
Pyruvate -> lactate
Pyruvate -> alanine

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3
Q

How is PFK1 regulated

A

Stimulated by AMP (muscle contract) and F-2,6-BP
Inhibited by ATP citrate (muscle relax)

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3
Q

Compare hexokinase and glucokinase

A

Hexokinase
- Product inhibited
- Muscles

Glucokinase
- Liver

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3
Q

Describe how is PK regulated

A

Low energy state
- Increase glucagon => phosphorylation into inactive PK => decrease PEP -> pyruvate

High energy state
- Increase insulin => dephosphorylation into active PK => increase PEP -> pyruvate

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3
Q

What is the pathophysiology of TCA cycle cofactor deficiencies

A
  • Thiamine deficiency => no TPP
  • Arsenic/Mecury poisoning inhibits lipoic acid

=> Decrease pyruvate DH and A-ketogluturate Dh activity => decrease ATP synthesis from TCA => Neurological damage & Organ failure

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4
Q

What are the effects of pyruvate carboxylase deficiency

A

Pyruvate accumulation => increase lactate => lactic acidosis & increase Acetyl CoA

Decrease oxaloacetate => decrease ATP & gluconeogenesis

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4
Q

What are the key steps of gluconeogenesis

A

Pyruvate -> Oxaloacetate (Pyruvate carboxylase)
Oxaloacetate -> PEP (PEP carboxylase)
F-1,6-BP -> F6P (F-1,6-BPase)
G6P -> Glucose (G6Pase)

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4
Q

How is pyruvate carboxylase regulated

A

Stimulated by Acetyl CoA
Inhibited by ADP

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4
Q

How is glycogen metabolism regulated hormonally in high energy states

A

Increase Insulin => bind to RTK => IRS phosphorylation => increase protein phosphatase 1 activity

  • Glycogen phosphorylase dephosphorylation
  • Glycogen synthase dephosphorylation

=> Glycogenesis > glycogenolysis

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4
Q

How is PEP carboxylase regulated

A

Stimulated by Glucagon => increased transcription
Inhibited by ADP

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5
Q

How is F-1,6-BPase regulated

A

Stimulated by Glucagon, Citrate & ATP
Inhibited by AMP & F-2,6-BP

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5
Q

What stimulates TCA cycle rate

A

Increase NAD+/ NADH ratio => increase TCA rate

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5
Q

Describe how aerobic exercise affects TCA rate

A

Increase O2 demand => Increase Oxphos => Increase NADH oxidised to NAD+ => increase NAD+/NADH => increase TCA cycle enzymes activity => increase ATP release

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6
Q

How is G6Pase regulated

A

Stimulated by Glucagon => increase transcription

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6
Q

How is glycogen metabolism regulated allosterically

A

Ca2+ release from sarcoplasmic reticulum => activates phosphorylase kinase => activates glycogen phosphorylase => increase glycogenolysis

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6
Q

How is glycogen metabolism regulated hormonally in low energy states

A

Increase Glucagon/Epinepherine => activate Gs protein => increase adenyl cyclase activity => increase ATP -> cAMP => increase PKA activity

  • Increase phosphorylase kinase phosphorylation => increase Glycogen Phosphorylase phosphorylation
  • Glycogen synthase phosphorylation

=> Glycogenolysis > glycogenesis

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6
Q

What is the pathophysiology of Von Gierke Disease

A

G6Pase deficiency
- Hyperuricaemia = G6P => HMP shunt
- Organomegaly = G6P buildup
- Lactic acidosis = G6P backflow => glycolysis => pyruvate => lactate
- Fasting hypoglycaemia = Glucose cannot be released from liver`

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6
Q

What is the pathophysiology of Andersen Disease

A

Branching enzyme deficiency
=> Long unbranched glycogen resistant to breakdown
- Liver, spleen accumulation => hepatosplenomegaly
- Liver failure & death

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6
Q

What is the pathophysiology of Cori Disease

A

4:4 transferase debranching enzyme deficiency
A-1,6-Glucosidase deficiency
=> glycogen cannot be fully broken down => decrease glucose release
- Fasting hypoglycaemia, weakness, hepatomegaly
- Abnormal branched glycogen structures

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6
Q

What is the pathophysiology of Pompe Disease

A

1-4 glucosidase deficiency in lysosomes
=> glycogen cannot breakdown => build up in lysosomes of muscles and heart => myopathy and cardiac failure

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6
Q

What is the pathophysiology of McArdle Disease

A

Glycogen phosphorylase deficiency in muscle
=> glycogen stuck in muscle => no glycogenolysis => no glycolysis => no pyruvate => no lactate
- Exercise intolerance
- Exercise-induced muscle pains and cramps

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7
Q

What are the functions of the different ETC complexes

A

Complex I = Reduced by NADH => e- flow and regenerate NAD+
Complex II = Reduced by FADH2
Complex IV = Reduces O2 -> H2O to accept e-

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7
What are the cofactors of pyruvate DH and A-ketoglutarate DH
Thiamine pyrophosphate (B1) Lipoic acid Coenzyme A (B5) FAD (B2) NAD+ (B3)
7
Which enzymes of the TCA release NADH
Isocitrate DH A-ketoglutarate DH Malate DH
8
How does the ETC generate ATP
Pumps H+ from Mt matrix to intermembrane space => H+ gradient across inner Mt membrane => ATP synthase allows H+ to enter matrix => energy used to phosphorylate ADP -> ATP
8
What are the relations of coenzyme Q to the ETC complexes
Complex I, II produce coenzyme Q Complex III uses coenzyme Q as a substrate
8
What is the effect of rotenone poisoning
Inhibits complex I
9
What is the function of uncoupling proteins and where are they found
Allows H+ to bypass ATP synthesis => produce energy as heat instead Found in brown fat
9
What is the effect of Antimycin A poisoning
Inhibits complex III
10
What is the effect of cyanide/ CO poisoning
Inhibits complex IV
10
What is the effect of dinitrophenol poisoning
H+ leakage
11
What is the pathophysiology of MELAS syndrome
Inactivating mutation in Mt tRNA - Decrease synthesis of ETC complexes => decrease ATP - Pyruvate and lactate buildup Myopathy, Encephalomyopathy, Lactic acidosis, Stroke-like episodes
11
What is the purpose of shuttlers in ETC
Transfer e- from cytosolic NADH to ETC as NADH cannot cross Mt membrane
12
What are the different ETC shuttlers and where are they found
Malate aspartate shuttle = Heart & liver Glycerol-3-phosphate shuttle = Skeletal muscles
13
Describe HMP shunt
G6P ->> nucleotide synthesis (G6PD) => produce NADPH antioxidant
14
What is the nature of G6PD deficiency
X-linked recessive
14
What is the pathophysiology of G6PD deficiency
Decrease NADPH => decrease glutathione => ROS and oxidative stress => haemolytic anaemia
14
What are the triggers of G6PD deficiency
Sulfa drugs Antimalarials Fava beans Infections
15
What are the signs of G6PD deficiency
Decrease Hb (normocytic) Increase reticulocytes Prehepatic jaundice => increase unconj. bilirubin and decrease haptoglobin
15
What is the histology for G6PD deficiency
Bite cells Heinz bodies
16
Describe the sources of glucose while fasted after a meal
0-6h = Mainly from dietary sources 6-24h = Mainly from liver glucogenolysis 24-72h = Mainly gluconeogenesis using AA as main substrates >72h = Gluconeogenesis + ketones
17
What is the pathophysiology of alcohol overdose
Ethanol metabolism => excess NADH => increase - Pyruvate -> lactate - DHAP -> glycerol-3-P => decrease gluconeogenesis => hypoglycaemia and lactic acidosis
17
Describe fatty oxidation
Activation to fatty acyl CoA => cartinine shuttle -> Mt (CPT1) => B-oxidation -> acetyl CoA => - Ketone bodies (ketogenesis) - TCA cycle
17
Explain if fatty acid oxidation and synthesis occur simultaneously
Do not occur simultaneously - Occur in different compartments - Malonyl-CoA inhibits CPT1 - High LCFA lvls inhibit Acetyl CoA carboxylase => decrease Malonyl CoA lvls
17
What happens when there is excess acetyl CoA and high energy demand
Ketogenesis takes over TCA as main energy producing process
17
Where is the location and regulation of Acetyl CoA carboxylase
Located in endoplasmic reticulum - Stimulated by Insulin and Citrate - Inhibited by Glucagon and Palmitoyl CoA
18
What are the different apolipoproteins
ApoE ApoA1 ApoC2 ApoB48 ApoB100
19
What is the function of ApoA1
Activates LCAT (only found on A-lipoproteins)
20
What is the function of ApoE
Mediates remnant uptake (except LDL)
20
What is the function of ApoC2
Lipoprotein lipase cofactor => catalyse cleavage
20
What is the function of ApoB48
Chylomicron secretion into lymphatics from intestines
20
What is the function of ApoB100
Binds LDL receptors (only on particles from liver)
20
How are lipids transported
Chylomicrons containing apoB48 enter lymphatics => enter blood stream and pick up apoC2 => apoc2 activates LPL, releases FA for tissues => chylomicron remnants and cholestrol cleared by liver w help of apoE Liver synthesis VLDL w apoB100 -> loses TG -> LDL => apoB100 binds to LDL receptors for LDL uptake => HDL apoA1 collects excess cholesterol from tissues and returns to liver
20
What is the pathophysiology of LDL-R/ApoB100 deficiency
Decrease circulatory LDL uptake and clearance => Increase LDL, cholesterol in blood
20
What is the pathophysiology of LPL/ApoC2 deficiency
Decrease TG breakdown of chylomicrons and VLDL into FFA by LPL (and apoC2) => increase Chylomicrons, TG, cholesterol in blood
20
How do resins decrease LDL-c
Bind bile salts and acids => inhibit reabsorption of bile => decrease bile salts pool in liver => increase liver cholesterol breakdown (to synthesise new bile acid) => increase in LDL-R expression and LDL clearance
21
What are the glycolytic intermediates of lipogenesis from carbohydrates
DHAP and pyruvate
21
What is the pathophysiology of ApoE deficiency
Decrease hepatic uptake of chylomicron remnants and cholesterol => increase chylomicrons, VLDL in blood
21
What are the effects of excess carbohydrate intake
Increase glycolysis => increase Acetyl CoA and Glycerol-3-phosphate => Liver FA, TG synthesis -> VLDL => increase VLDL lvls
21
What are the effects of low carbohydrate intake
Decrease insulin => body switches to fat metabolism => increase B-oxidation => ketone bodies - Acidosis - Fruity breath smell (acetone)
21
What are the 9 essential amino acids
Phenylalanine Valine Tryptophan Threonine Isoleucine Methionine Histidine Arginine Lysine Leucine
21
What are the branched chain amino acids
Isoleucine Leucine Valine
21
Which amino acids are purely ketogenic
Lysine and Leucine
21
What is the pathophysiology of Maple Syrup Urine Disease
Impaired BCAA breakdown => increase BCAAs in urine - Syrup smelling urine - Intellectual disability - Poor oral intake
21
What is the pathophysiology of phenylketonuria
- Phenylalanine Hydroxylase deficiency => Phenylalanine accumulation & Tyrosine deficiency - High phenylpyruvate inhibits pyruvate carboxylase in brain => mental retardation
22
What is the treatment of phenylketonuria
Tyrosine supplements
22
What is the MOA of allopurinol
- Hypoxanthine analogue & competitive xanthine oxidase inhibitor - Inhibits PRPP amidotransferase activity => decrease PRPP - Forms allopurinol ribonucleotide => decrease intracellular PRPP
22
Does allopurinol cause hypoxanthine accumulation
No. HGPRT converts hypoxanthine => IMP
23
What are the effects of allopurinol
IMP and XMP accumulation Xanthine and Hypoxanthine excretion
24
What is the treatment for paracetamol toxicity and its MOA
N-acetylcysteine Replenishes glutathione => inactivates toxic metabolites
25
What is the pathophysiology of Severe Combined Immunodeficiency DIseases
Ribonucleotide Reductase inhibited => ADA deficiency and increase dATP => inactivated RNR => decrease DNA synthesis => decrease T & B cell replication
26
What is the pathophysiology of diabetic ketoacidosis
Insulin deficiency => unopposed glucagon action - Activated HSL => increase lipolysis - Inhibited Acetyl CoA carboxylase => increase lipogenesis => Increase B oxidation -> acetyl coA => increase ketogenesis -> ketone bodies => decrease pH and acidosis
26
How do the presentations of DKA come about
Increase blood glucose => exceed renal threshold => osmotic diuresis - Increase osmolality - Dehydration and polyuria Increase protein breakdown => Increase urea - Weight loss (protein breakdown) - Altered mental state Increase lipolysis => Hyperlipidemia and increased ketone bodies - Sweet fruity breath - Metabolic acidosis (low pH and HCO3-) - Kussmaul breathing (hyperventilation)
27
What are the lab tests done to diagnose diabetes
- Fasting glucose >/= 7.0 mmol/L - 2h oral glucose tolerance test, random glucose >/= 11.1mmol/L - HbA1c >/= 6.5%
28
What are the lab tests done to distinguish type 1 DM from type 2 DM
- C-peptide decreased - Islet autoantibodies eg glutamic acid decarboxylase
29
What is the treatment for diabetic ketoacidosis
Attend to airway, breathing, circulation Fluid replacement Insulin replacement Antibiotics Heparin
30
Why is fluid replacement done before insulin replacement for DKA
Insulin increases glucose uptake => shifts osmotic gradient => water to enter compartment - Circulatory collapse - Cerebral edema
31
What are the criteria for determining metabolic syndrome
At least 3 - Increase waist circumference - Increase blood fasting glucose - Increase blood TG - Increase HDL-c - Hypertension
32
What is the pathophysiology of type 2 diabetes
Increase visceral fat => releases inflammatory cytokines and FFA => FFA impairs insulin signalling in liver and muscle => decrease glucose uptake and hepatic gluconeogenesis suppression => increase blood glucose

Tung Tung Tung Tung Sahur (4 decks)

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