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FOO > THE PATHOPHYSIOLOGY OF THE REFEEDING SYNDROME > Flashcards

THE PATHOPHYSIOLOGY OF THE REFEEDING SYNDROME Flashcards

1
Q

ROLE OF PYRUVATE CARBOXYLASE IN CONTEXT OF GLUCONEOGENESIS?

A

IT ACTIVATES IT; it catalyzes the carboxylation of pyruvate to oxaloacetate, which is the precursor for the biosynthesis of many C4 intermediates and is used in gluconeogenesis

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2
Q

WHICH MOLECULE ACTIVATES PYRUVATE CARBOXYLASE AND THUS HELPS ACTIVATE GLUCOENEOGENESIS?

A

ACETYL CoA

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3
Q

GLUCOSE PARADOX REFERS TO?

A

DELAYS IN RETURN TO NORMAL METABOLISM UPON REFEEDING AFTER A PERIOD OF STARVATION; CHARACTERISED BY THE CONTINUED HIGH RATES OF GLUCONEOGENESIS EVEN THOUGH THERE IS PLENTY OF GLUCOSE BEING INGESTED

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4
Q

WHAT IS GLYCONEOGENESIS?

A

SYNTHESIS OF GLYCOGEN WITHOUT USING GLUCOSE OR OTHER CARBS AND USING PROTEINS, FATS ETC. INSTEAD

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5
Q

EXAMPLES OF NON CARBOHYDRATES THAT THE LIVER CAN CONVERT INTO GLYCOGEN?

A

ALL THAT CAN BE USED IN GLUCONEOGENESIS (LACTATE, PYRUVATE, GLYCEROL, GLUCOGENIC AMINO ACIDS)

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6
Q

INITIAL REFEEDING STAGE IS CHARACTERISED BY HIGH RATES OF GLUCONEOGENESIS (AND GLYCONEOGENESIS). HOW IS THIS MAINTAINED?

A
  • PYRUVATE CARBOXYLASE THAT ACTIVATES GLUCONEOGENESIS IS KEPT ACTIVATED DURING THE INITIAL STAGES
  • IT IS ACTIVATED BY HIGH RATES OF ACETYL CoA
  • ACETYL CoA ALSO INHIBITS PYRUVATE DEHYDROGENASE, SO THE PYRUVATE ITSELF CAN’T GO TO ACETYL CoA
  • IN ODER TO MAINTAIN THIS CONTINUED ELEVATION OF ACETYL CoA, A HIGH RATE OF FATTY ACID OXIDATION IS NEEDED WHICH IS PARADOXAL TO REFEEDING PROCESS, SINCE THERE ARE NUTRIENTS COMING FROM THE INGESTION
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7
Q

IN EXPERIMENTS ON RATS, HOW LONG DO THE HIGH RATES OF FAT OXIDATION STAY MAINTAINED AFTER INITIAL REFEEDING?

A

3-4 HRS

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8
Q

HOW MUCH TIME AFTER REFEEDING DOES THE RETURN TO METABOLISM WHICH RESEMBLES THE FED STATE OCCUR?

A

6-9HRS

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9
Q

HOW DOES THE LIVER ACQUIRE FATS FOR FATTY ACIDS OXIDATION UPON REFEEDING WHEN THE INGESTED FOOD LEADS TO RISE IN INSULIN LEVELS AND THEREFORE INHIBITION OF LIPOLYSIS?

A

THE LIVER HAS TO OXIDISE FATTY ACIDS GENERATED THROUGH LIPOLYSIS OF ITS OWN, ENDOGENOUS TRIGLYCERIDES

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10
Q

LEVELS OF TRIGLYCERIDES IN HEPATOCYTES DURING STARVATION ARE LOW OR HIGH?

A

HIGH

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11
Q

FED STATE VS FASTED STATE VS REFEEDING; COMPARE THE AMOUNT OF FATTY ACIDS SECRETED BY THE LIVER?

A

FED STATE; HIGHEST PROPORTION OF FATTY ACIDS SECRETED FROM THE LIVER AS IT IS NOT HEALTHY/NORMAL FOR THEM TO ACCUMULATE THERE. SECRETED IN A FORM OF VLDL TO BE STORED IN ADIPOSE TISSUE
FASTED STATE; THE PROPORTION OF FATTY ACIDS SECRETED FROM THE LIVER DECREASES
REFEEDING; AMOUNT OF TRIGLYCERIDES THAT THE LIVER SECRETES DECREASES MORE BECAUSE IT’S TRYING TO RETAIN THEM FOR ITSELF TO THE HEPATOCYTES CAN OXIDISE THEM AND MAINTAIN MITOCHONDRIAL ACETYL CoA CONCENTRATIONS AND ATP FORMATION

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12
Q

HOW LONG AFTER THE REFEEDING DOES THE LIVER START RELEASING TRIGLYCERIDES AT A HIGH RATE AGAIN?

A

3-4 HRS

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13
Q

WHAT HAPPENS TO INGESTED GLUCOSE DURING THE FIRST 3-4 HRS AFTER REFEEDING?

A

A MINORITY GOES DIRECTLY TO THE LIVER TO FORM GLYCOGEN
MAJORITY OF GLUCOSE HOWEVER GOES TO THE PERIPHERY, ESP THE LARGEST INSULIN SENSITIVE TISSUE (SKELETAL MUSCLE) WHERE IT IS CONVERTED INTO LACTATE, RELEASED INTO THE BLOOD AND THEN TAKEN UP BY LIVER TO FORM GLYCOGEN AND REESTABLISH GLYCOGEN RESERVES

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14
Q

WHAT IS LIVER’S SOURCE OF ATP DURING REFEEDING?

A

FATTY ACIDS

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15
Q

GLYCOGEN STORES IN THE LIVER ARE REPLENISHED HOW LONG AFTER REFEEDING?

A

3-4 HRS

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16
Q

GLYCOGEN REPLETION DURING REFEEDING MAINLY OCCURS THROUGH DIRECT OR INDIRECT PATHWAY?

A

INDIRECT (GLUCOSE-PYRUVATE-LACTATE-GLYCOGEN)

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17
Q

HOW IS THE PYRUVATE KINASE STEP (PEP TO PYRUVATE) BYPASSED IN GLUCONEOGENESIS?

A

BY FORMATION OF OXALOACETATE FROM PYRUVATE BY PYRUVATE CARBOXYLASE. OXALOACETATE CAN THEN BE CONVERTED BACK INTO PEP.

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18
Q

WHICH ENZYME IS RESPONSIBLE FOR BYPASSING PFK1 STEP DURING GLUCONEOGENESIS?

A

F-1,6-BIPHOSPHATASE

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19
Q

WHICH METABOLITE REGULATES PFK1 AND F16BPASE AND HOW?

A 
FRUCTOSE 2,6 BIPHOSPHATE
ACTIVATES PFK1 (AND GLYCOLYSIS)
INHIBITS F16BPASE (AND GLUCONEOGENESIS)
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20
Q

WHAT ARE THE RATES OF F2,6BIPHOSPHATE LIKE DURING INITIAL PHASES OR REFEEDING AND WHY?

A

THEY ARE MAINTAINED LOW SO THE PFK1 ACTIVITY REMAINS LOW AND GLYCOLYSIS ISN’T ACTIVATED + F1,6BIPHOSPHATASE IS HIGH AND GLUCONEOGENESIS IS MAINTAINED

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21
Q

HOW LONG DO THE RATES OF F2,6BIPHOSPHATE REMAIN LOW DURING INITIAL REFEEDING?

A

PERIOD OF 4 HRS

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22
Q

LIVER GLYCOGEN IS ALMOST FULLY REPLETED WITHIN HOW MANY HRS OF REFEEDING?

A

5HRS

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23
Q

WHAT PERCENTAGE OF GLUCOSE DURING EARLY STAGES OF REFEEDING IS COMING FROM GLUCONEOGENESIS FROM SUBSTRATES LIKE LACTATE?

A

75%

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24
Q

HOW DOES INSULIN AFFECT GLYCOGEN SYNTHESIS?

A

DIRECTLY STIMULATES THE LAST STEP IN GLYCOGEN SYNTHESIS; THE ENZYME GLYCOGEN SYNTHETASE

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25
Q

DOES THE LIVER EVER RELEASE GLYCOGEN?

A

NO, IT ALWAYS BREAKS IT DOWN TO GLUCOSE FIRST AND THEN RELEASES IT INTO THE BLOODSTREAM

26
Q

2 PARADOXES IN HEPATIC METABOLISM DURING REFEEDING?

A

1) HIGH RATES OF GLYCONEOGENESIS (GLUCOSE FROM THE DIET GOES TO PYRUVATE AND LACTATE AND IS THEN USED BY LIVER TO REESTABLISH GLYCOGEN STORES, HIGH RATES OF FATTY ACID OXIDATION ACCOMPANY THIS)
2) F26bPHOSPHATE LEVELS ARE LOW SO PFK1 ISN’T ACTIVATED SO GLYCOLYSIS ISN’T ACTIVATED EITHER (BUT F1,6BIPHOSPHATASE IS ACTIVATED WHICH DRIVES GLUCONEOGENESIS)

27
Q

WHAT IS THE CAUSE OF THE ‘REFEEDING SYNDROME’?

A

PATIENTS BEING REFED TOO QUICKLY ON AN UNBALANCED HIGH CARBOHYDRATE DIET

28
Q

MAIN PATHOPHYSIOLOGICAL FEATURES OF THE REFEEDING SYNDROME ARE:

A

ELECTROLYTE IMBALANCES;
HYPOPHOSPHATAEMIA (LOW PHOSPHATE)
HYPOKALAEMIA (LOW POTASSIUM)
HYPOMAGNESAEMIA (LOW MAGNESIUM ION CONCENTRATIONS)

29
Q

DESCRIBE THE PATHOPHYSIOLOGICAL CHANGES THAT OCCUR IN THE REFEEDING SYNDROME?

A
  • ELECTROLYTE IMBALANCES (LOW K, Mg and P)
  • ALTERED FLUID BALANCE BECAUSE INSULIN THAT’S NOW BEING SECRETED PROMOTES Na+ AND GLUCOSE REABSORPTION IN THE KIDNEY TUBULES AND THIS RESULTS IN INCREASED WATER RETENTION (WATER FOLLOWS Na+)
  • GLUCOSE METABOLISM REQUIRES PHOSPHORYLATION OF MANY INTERMEDIATES; THE USE OF INDIRECT PATHWAY TO REPLENISH HEPATIC GLYCOGEN MEANS THERE IS A LARGE SCALE PHOSPHATE ION UPTAKE INTO INSULIN SENSITIVE GLUCOSE-METABOLISING TISSUES
30
Q

DURING THE REFEEDING SYNDROME, THERE IS A VERY LARGE DEMAND FOR WHICH ION?

A

PHOSPHATE

31
Q

DEFICIENCY IN WHICH VITAMIN IS PARTICULARLY EXAGGERATED DURING THE REFEEDING SYNDROME AND WHY?

A

THERE IS ALREADY A DEFICIENCY OF MOST VITAMINS DURING STARVATION BUT VIT B 1 (THIAMINE) IS EXAGGARATED BECAUSE IT NEEDS TO BE PHOSPHORYLATED INTO ITS ACTIVE FORM (THIAMINE PYROPHOSPHATE, TPP). SO THE STARVED INDIVIDUAL ALREADY STARTS WITH A DEFICIT IN ADDITION TO HYPOPHOSPHATAEMIA THAT OCCURS DURING REFEEDING WHICH REDUCES TPP FORMATION

32
Q

HOW IS VIT B1 (THIAMINE) ACTIVATED AND WHAT’S THE ACTIVE FORM CALLED?

A

BY BEING PHOSPHORYLATED

THIAMINE PYROPHOSPHATE, TPP

33
Q

PATIENTS WHO ARE MOST SUSCEPTIBLE TO REFEEDING SYNDROME:

A
  • THOSE SUFFERING FROM ANOREXIA NERVOSA
  • CHRONIC MALNUTRITION
  • ALCOHOLISM
  • CHRONIC VOMITTING OR DIARRHOEA
  • POST WEIGHT-LOSS SURGERY
  • ONCOLOGY PATIENTS WITH CANCER CACHEXIA
  • OTHER MAJOR SURGERIES
34
Q

WHAT IS CACHEXIA?

A

EXTREME WEIGHTLOSS AND MUSCLE WASTING

35
Q

HOW DOES HYPOKALAEMIA OCCUR IN THE PLASMA DURING REFEEDING?

A
  • THE HIGH INSULIN LEVELS RESPONDING TO CARBOHYDRATE INTAKE ACTIVATE THE Na+-H+ ANTIPORTER (SO SODIUM IS TAKEN INTO THE CELLS IN EXCHANGE FOR PROTONS=
  • THIS INCREASE IN INTRACELLULAR SODIUM INCREASES THE ACTIVITY OF Na+K+ATPASE AT THE CELL MEMBRANE (A PUMP WHICH USES ATP)
  • THE PUMP KEEPS EXCHANGING INTRACELLULAR Na+ FOR EXTRACELLULAR K+
  • AS Na+ CONCENTRATIONS INCREASE, THE PUMP ACTIVITY INCREASES AND MORE K+ IS TAKEN UP INTO THE CELLS AGAINST ITS CONCENTRATION GRADIENT, RESULTING IN HYPOKALAEMIA
36
Q

WHY ARE THE PLASMA LEVELS OF PHOSPHATE LOW IN REFEEDING SYNDROME?

A

IF THERE IS SUDDENLY EXTENSIVE AMOUNT OF GLUCOSE METABOLISM (WHICH REQUIRES A LOT OF PHOSPHORYLATION) HAPPENING IN THE PERIPHERY, THE Na+–PO4 3- COTRANSPORTER (WHICH TRANSPORTS PHOSPHATE INTO CELLS) GETS ACTIVATED TO THAT EXTENT THAT IT LEADS TO HYPOPHOSPHATAEMIA

37
Q

WHICH TRANSPORTER TRANSPORTS PHOSPHATE INTO CELLS?

A

Na+ — PO4 3- CONTRANSPORTER

38
Q

WHAT IS THE MOST ACTIVE FORM OF VIT D IN THE BODY?

A

1,25 DIHYDROXYL VIT D

39
Q

IN WHICH FORM IS PHOSPHATE STORED IN THE BONE?

A

CALCIUM PHOSPHATE

40
Q

IS PHOSPHATE AN ACID OR A BASE?

A

A BASE; IT WILL REMOVE PROTONS FROM A SOLUTION

41
Q

WHY IS PHOSPHATE CONCENTRATION IN THE BLOOD NORMALLY MAINTAINED WITHIN A NARROW RANGE?

A

BECAUSE IF IT’S TOO HIGH IT WILL LEAD TO TOO MUCH CALCIFICATION (E.G. IN BLOOD VESSELS WALL) AND IF IT IS TOO LOW IT STARTS BEING RELEASED FROM BONE LEADING TO OSTEOPOROSIS

42
Q

COMPOSITION OF PHOSPHOLIPIDS (CELL MEMBRANE COMPONENTS):

A
  • A CHARGED BASE
  • A PHOSPHATE GROUP
  • A GLYCEROL BACKBONE WITH 2 FATTY ACID CHAINS
43
Q

HOW MANY FATTY ACID CHAINS ARE THERE IN A PHOSPHOLIPID MOLECULE?

A

2

44
Q

WHAT IS THE ADVANTAGE OF PHOSPHORYLATING ALL SUGARS AND CELLULAR INTERMEDIATES?

A

ONCE PHOSPHORYLATED THEY BECOME IMPERMEABLE THROUGH THE LIPID BILAYER (IT HAS RICH HYDROPHOBIC CORE THAT PHOSPHATE AS A CHARGED ENTITY DOESN’T CROSS SPONTANEOUSLY). PHOSPHORYLATED METABOLITES (E.G. GLUCOSE TO G6P) STAY WITHIN THE CELL AND CAN BE METABOLISED AS REQUIRED

45
Q

PHOSPHORYLATION KEEPS METABOLITES WITHIN THE CELL OR ALLOWS THE TO LEAVE THE CELL?

A

KEEPS THEM WITHIN

46
Q

WHAT IS ANOTHER DIRECTION GLUCOSE CAN BE METABOLISED IN ADDITION TO GLYCOLYSIS AND WHAT IS THIS PATHWAY IMPORTANT FOR?

A

PENTOSE PHOSPHATE PATHWAY, IMPORTANT FOR DNA AND RNA SYNTHESIS

47
Q

WHAT IS 2,3 DPG AND HOW IS IT ALTERED DURING REFEEDING SYNDROME?

A
  • IN ERYTHROCYTES
  • A METABOLITE THAT CHANGES HEMOGLOBIN KINETICS AND REDUCES ITS AFFINITY FOR OXYGEN WHEN IT ERYTHROCYTES REACHES TISSUES THAT NEED OXYGEN AND PRODUCE CO2
  • PHOSPHATE IS IMPORTANT FOR SYNTHESIS OF THIS METABOLITE
  • HYPOPHOSPHATAEMIA IS A CHARACTERISTIC OF THE REFEEDING SYNDROME
  • THIS LEADS TO INSUFFICIENT SUPPLY OF OXYGEN TO SOME TISSUES
  • CAN LEAD TO VARIOUS SYMPTOMS, E.G. COGNITIVE DYSFUNCTION IN THE BRAIN
48
Q

HYPOPHOSPHATAEMIA INHIBITS TPP FORMATION. WHAT ARE SOME ROLES OF TPP THAT WILL BE LOST BECAUSE OF THIS?

A
  • TPP IS REQUIRED FOR PYRUVATE DEHYDROGENASE ACTIVITY (PYRUVATE TOACETY CoA)
  • REQUIRED IN METABOLISM OF BRANCH-CHAIN AMINOACIDS
  • TPP IS A CO FACTOR FOR AN ENZYME IN TCA CYCLE
  • INVOLVED IN GLUTAMATE REGULATION (GLUTAMATE IS A NEUROTRANSMITTER SO THIS WILL RESULT IN NEURAL SYMPTOMS)
49
Q

IS ATP SYNTHESISED DURING GLUCOENEOGENESIS?

A

NO

50
Q

IS TPP ABSORBED IN THE GUT?

A

NO, INACTIVE FORM OF VIT B1 (THIAMINE) IS ABSORBED IN THE GUT AND THEN PHOSPHORYLATED TO MAKE TPP

51
Q

BLOOD VOLUME AND BODY WATER ARE INCREASED OR DECREASED DURING THE REFEEDING SYNDROME?

A

INCREASED (DUE TO ELECTROLYTE IMBALANCE, MORE Na+ REUPTAKE IN THE KIDNEY DUE TO INSULIN SO MORE WATER RETENTION)

52
Q

SODIUM ION REABSORPTION IS INTEGRATED WITH THE REABSORPTION OF WHICH MOLECULE BY THE KIDNEY?

A

GLUCOSE

53
Q

SGLT2 TRANSPORTER; HOW IS IT ACTIVATED, RATIO OF Na+:GLUCOSE IT TRANSPORTS, AFFINITY FOR GLUCOSE?

A
  • ACTIVATED BY INSULIN
  • TRANSPORTS Na+ and GLUCOSE IN 1:1 RATIO
  • RELATIVELY LOW AFFINITY FOR GLUCOSE
54
Q

IF THE BLOOD GLUCOSE EXCEEDS WHAT LEVEL IT STARTS ACCUMULATING IN URINE?

A

11 mmol/L

55
Q

WHY DOES SLGT1 HAS MUCH BIGGER AFFINITY FOR GLUCOSE THAN SGLT2?

A

BECAUSE IT IS LOCATED FURTHER ALONG THE TUBULES IN THE KIDNEYS THAN SGLT2 WHERE THE AMOUNT OF GLUCOSE IN THE FILTARTE HAS ALREADY BEEN DECREASED SUBSTANTIALLY

56
Q

WHICH SGLT, 1 OR 2 IS NOT ACTIVATED BY INSULIN?

A

SGLT1

57
Q

IN WHICH RATIO DOES SGLT1 TRANSPORT GLUCOSE AND SODIUM?

A

1:2

58
Q

DOES THE REFEEDING SYNDROME OCCUR IN ENTERAL OR PARENTERAL FEEDING MORE?

A

ENTERAL

59
Q

IF ELECTROLYTE SERUM LEVELS ARE NORMAL PRIOR TO REFEEDING CAN WE ASSUME LOW RISK OF REFEEDING SYNDROME AND WHY?

A

NO BECAUSE SERUM LEVELS MIGHT STILL BE NORMAL DESPITE BODY DEPLETION

60
Q

HYDRATING A PATIENT WITH GLUCOSE OR Na+ BASED LIQUIDS DURING REFEEDING WILL HAVE WHAT KIND OF EFFECTS ON THE PATIENT?

A

IT WILL EXACERBATE REFEEDING SYNDROME SYMPTOMS (MOSTLY RISE IN BLOOD Na+ AND HYPOPHOSPHATAEMIA)

61
Q

REFEEDING SYNDROME CAN LEAD TO WHICH COMPLICATIONS?

A
  • WEAKNESS AND PARALYSIS IN MUSCLE
  • LACTIC ACIDOSIS
  • CONGESTIVE HF
  • PULMONARY OEDEMA..

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